RAx4hvubM2 ZZRE1ta6uxFCiV1fyrtQgthsJZDhMI6YAs
has assertion: a(CHEBI:gemcitabine) -> r(HGNC:SLC25A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.177+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gemcitabine) -> r(HGNC:SLC25A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15837765

BEL Framework Large Corpus Document
description: Approximately 61,000 statements.
rights: Copyright (c) 2011-2012, Selventa. All rights reserved.
authored by: Selventa
version: 1.4

3
value: Table 1. Genes relatively overexpressed in gemcitabine-sensitive pancreatic cancer cell lines
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15837765

RA70P-UcamLD9IDdP MkutpOCVBYEzHOeUMG-FkrJE78Y
has assertion: a(CHEBI:gemcitabine) -> r(HGNC:SERPINF2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.178+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gemcitabine) -> r(HGNC:SERPINF2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15837765

3
value: Table 1. Genes relatively overexpressed in gemcitabine-sensitive pancreatic cancer cell lines
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15837765

RA3o2QeqPJrPt1vt py2-o gLuQpdQf1hVKGUink9-G0s
has assertion: tscript(p(MGI:Srf)) -| p(MGI:Cfl1,pmod(P,S,3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.186+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Srf)) -| p(MGI:Cfl1,pmod(P,S,3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15837932

5
value: At the posttranslational level, cofilin, a key regulator of actin dynamics, displays dramatically elevated inhibitory phosphorylation at Ser-3.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15837932

RA4GTY4TPpryXnIVwASyEAKkTr4s1wzcQxhH3IsKdyQU4
has assertion: p(HGNC:TNF) -> p(EGID:183)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.187+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(EGID:183)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15837949

4
value: TNF-alpha (P also increased angiotensinogen and angiotensin II in isolated adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15837949

RA4KV iZkkqkMtc0RvpVzr1Os1bon YdTGhTaBbPU8VKc
has assertion: p(HGNC:TNF) -> tscript(complex(NCH:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.188+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> tscript(complex(NCH:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15837949

4
value: TNF-{alpha} induces transcription of AGT via the transcription factor nuclear factor-{kappa}B, which is known to be involved in the production of numerous proinflammatory markers.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15837949

RA3v2XrV5fpKNtEjB8vvxLy-zyDWL6Oum75ADB7eGN2xI
has assertion: kin(p(MGI:Prkcb)) -> p(MGI:Tnni3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.192+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Prkcb)) -> p(MGI:Tnni3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840586

5
value: Although both PKCbetaII and PKCepsilon can phosphorylate cTnI
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840586

RA0J2BGNIN5-q7Yj6eSfKdPiLvlYWxqSNnZZr3y19uluI
has assertion: kin(p(PFM:"Prkc Family")) -> p(MGI:Tnni3,pmod(P,S))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFM:"Prkc Family")) -> p(MGI:Tnni3,pmod(P,S))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840586

5
value: Protein kinase C (PKC)-induced phosphorylation of cardiac troponin I (cTnI)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840586

RA7W72IakcW3P-6PCoNUOlfyWAhUWCCMEAc8ZY7bvFHvg
has assertion: bp(GO:angiogenesis) -> r(HGNC:ARF6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.204+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:ARF6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA9cShioU88Ig-nthQMmBZjt56JzPWoK2ne5KHlkyZsY0
has assertion: bp(GO:angiogenesis) -> r(HGNC:ARHGAP5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.206+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:ARHGAP5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAzjB4-I3OU0o RVoXSNs43xgUOVkWiMVvP-WYrQWy0R4
has assertion: bp(GO:angiogenesis) -> r(HGNC:ARHGAP18)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.211+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:ARHGAP18)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA3d94mL286V 6LvZbLeGKESIuaP2-7oEGGxXr9dcrDz0
has assertion: bp(GO:angiogenesis) -> r(HGNC:CD59)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.216+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:CD59)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAyaOZnIhtVbpQufcML HlMwwy45m3JLGtBNnvVyBadAY
has assertion: bp(GO:angiogenesis) -> r(HGNC:CXCR4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.220+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:CXCR4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA4cuZ KX 5knf4iz1XlzOZFGBoLFRsKrJsq6ptLR AZw
has assertion: bp(GO:angiogenesis) -> r(HGNC:CBFB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.222+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:CBFB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA8nnjUOxYztl8PGJ16x7eOzXgPEwLaYp0X4rSwx-rdnA
has assertion: bp(GO:angiogenesis) -> r(HGNC:ETS1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.232+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:ETS1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAywYpNBqHdnZaf KSdv3-US2kz Fa7vXL8uowqmsRgdw
has assertion: bp(GO:angiogenesis) -> r(HGNC:IPO7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.247+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:IPO7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA8L6xFqNlaGVjuT9GAPcAqH7AKfbEXbrBy4IGixaa6wA
has assertion: bp(GO:angiogenesis) -> r(HGNC:JUNB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.252+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:JUNB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA0wj8mfqf2sUUNitm6efhxEhmeljF1bVWaJMbjqlKVfw
has assertion: bp(GO:angiogenesis) -> r(HGNC:MAP3K1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.261+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:MAP3K1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA5AiJgDrCi-3GC0MPTV3NZF yyNDnyhCKfi7aMvL4scU
has assertion: bp(GO:angiogenesis) -> r(HGNC:PPAP2B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.275+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:PPAP2B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAz5-BHBpJnYQ32TnEObfy1N PV6TKNWOhZrMiso2lJnw
has assertion: bp(GO:angiogenesis) -> r(HGNC:RAB6C)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.279+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:RAB6C)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAyK3YkJMMVfmTF9E ZpuHRUmrexR15TOAa-vZSTo11Ao
has assertion: bp(GO:angiogenesis) -> r(HGNC:RAN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.285+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:RAN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA9Kd5x7NzGyURSCqNkpGZfnU6Egjua1m2YWeFKQ61CjQ
has assertion: bp(GO:angiogenesis) -> r(HGNC:REST)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.288+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:REST)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAx1Nzo8RFYrdj1KJZFToy3AIFmHqxsqHdGKs1Wn3qIAg
has assertion: bp(GO:angiogenesis) -> r(HGNC:RHOB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.289+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:RHOB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA7Z4654dj KJwa9orEc3YUHMVKt6mpHjDcrvyo4kxuu0
has assertion: bp(GO:angiogenesis) -> r(HGNC:RIN2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.290+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:RIN2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA80v-QA jb8 t87iAexR3NIchbI7sy38DlfPAm5hLTg0
has assertion: bp(GO:angiogenesis) -> r(HGNC:SELE)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.292+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SELE)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA9ye5cxSs9FliACswaVqO20bvCKeVJwKdqLbzPfWKM3c
has assertion: bp(GO:angiogenesis) -> r(HGNC:SERPINB2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.294+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SERPINB2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA-bSKdobXxr4gSg5cwFC-v-Y96wG2n3-7ZESV5962KeI
has assertion: bp(GO:angiogenesis) -> r(HGNC:SERPINE2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.295+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SERPINE2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAywdaekR43o AQtu95hgTK-TApoQqtpKlrGr0Te3M3 0
has assertion: bp(GO:angiogenesis) -> r(HGNC:SLC19A2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.297+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SLC19A2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA0Bx8I0zkPn0iesW3zHbU9G7L2WwovgEilm9QdrjNSBQ
has assertion: bp(GO:angiogenesis) -> r(HGNC:SLC38A2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.298+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SLC38A2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA5QnIAsAKRp2vaU7S7qNIQBxToU012UVrZONKnKkHFvE
has assertion: bp(GO:angiogenesis) -> r(HGNC:SUMO1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.302+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:SUMO1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA3AdrSsI N8xOkVVl-OZxfVw-P1yUC9DN8v4HH5UMfYk
has assertion: bp(GO:angiogenesis) -> r(HGNC:TCF4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.308+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:TCF4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA6jaXOEpiNqSGGTY2QHnfTI5B7LKeLBStVR7X8rskS9o
has assertion: bp(GO:angiogenesis) -> r(HGNC:TM4SF1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.312+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:TM4SF1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA8zxxtsfT 214Vfm7OiWe74hB7beUlubERi2p7Hb2r-I
has assertion: bp(GO:angiogenesis) -> r(EGID:81671)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.314+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(EGID:81671)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAxsm8FgiV1LGwzZ4tgUhwQI08ao5k4H95XdifGTWcYxg
has assertion: bp(GO:angiogenesis) -> r(HGNC:UBE2D1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.316+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:UBE2D1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAyC6w 9esRy-ZT4hnoV ZTSbOBHrcXVgJLvGAKayTlOQ
has assertion: bp(GO:angiogenesis) -> r(HGNC:UBQLN1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.317+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:UBQLN1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA9TQKtjNSCdPI9-HuRUpX3gmMhndmaP5cQbFYp02e2K4
has assertion: bp(GO:angiogenesis) -> r(HGNC:USP7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.318+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -> r(HGNC:USP7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: Fig. 4. Genes regulated during capillary tube formation. upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA48brA8paeReYedTuEbKRyiNHFihxb0N7GJV0 H nkZQ
has assertion: bp(GO:angiogenesis) -| r(HGNC:"MT-ND4L")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.328+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -| r(HGNC:"MT-ND4L")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA3hKo18Evk-V6mrHXC6pjz q-iyl-HIUSZGMh4RntvCI
has assertion: bp(GO:angiogenesis) -| r(HGNC:OXA1L)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.329+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -| r(HGNC:OXA1L)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAxty8mi0Q8hRtjRsstSS39jJlZZH3p4q-m9enf8D1UgQ
has assertion: bp(GO:angiogenesis) -| r(HGNC:"MT-CO1")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.333+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -| r(HGNC:"MT-CO1")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RAzXDCrZPrEiq1lb5sPfVj75EM6jUymm0ovaN9-gIYngM
has assertion: bp(GO:angiogenesis) -| r(HGNC:"MT-CYB")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.334+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:angiogenesis) -| r(HGNC:"MT-CYB")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15840639

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15840639

RA O4UCyE3NR2Coheo2qK7mKmHH37tdeIlD3L4wVVgWcQ
has assertion: path(MESHD:Hyperoxia) -> r(MGI:Bcl2a1b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.336+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Hyperoxia) -> r(MGI:Bcl2a1b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15841185

3
value: A1 was induced in hyperoxia
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15841185

RA0Z5sJfes3o1IHBasfqrfvBaXrYbCkmHVtubqBy8AsO4
has assertion: p(MGI:Vegfa) -| (path(MESHD:Hyperoxia) -> bp(GO:"cell death"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.341+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Vegfa) -| (path(MESHD:Hyperoxia) -> bp(GO:"cell death"))
label: path(MESHD:Hyperoxia) -> bp(GO:"cell death")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15841185

4
value: VEGF also conferred protection via an A1-dependent mechanism
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15841185

RA5cdwuLvWYWmCJoXX4r 8fd-p64iy2sbxxkLZgh7rP0Q
has assertion: bp(GO:"complement activation") -> path(SDIS:"tissue damage")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.343+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"complement activation") -> path(SDIS:"tissue damage")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15841213

2
value: TNFR1 promotes systemic immune responses and renal T cell death, while intrinsic cell TNFR2 plays a critical role in complement-dependent tissue injury.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15841213

RA-xwZoCWJmOsKWbIdfRtkiJ4pBH04ucjFNzh4fzM1N6I
has assertion: bp(GO:"response to hypoxia") -> r(EGID:104263)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.349+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(EGID:104263)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15843612

3
value: Table 3. Genes changed after hypoxia that are unique to HIF1A WT upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15843612

RAw7CJQloiD8JFyx5jQSywppP8OkxPGxE6OjWQ iWflWY
has assertion: bp(GO:"response to hypoxia") -> r(MGI:Pim3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.389+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(MGI:Pim3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15843612

3
value: table 2 - genes changed after hypoxia common to HIF1A WT and HIF1A del upregulated by hypoxia
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15843612

RA5XUIPtvUuSwhIV6-qWCkP6n1XW4ZIpR1Rho2thvFxdI
has assertion: bp(GO:"response to hypoxia") -> r(MGI:Sesn1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.396+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(MGI:Sesn1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15843612

3
value: table 2 - genes changed after hypoxia common to HIF1A WT and HIF1A del upregulated by hypoxia
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15843612

RA0R RbxcZYvXKheI9zhiC0XeLi5U99842MoX8NFJbdRU
has assertion: bp(GO:"response to hypoxia") -> r(MGI:Smad1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.397+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(MGI:Smad1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15843612

3
value: table 2 - genes changed after hypoxia common to HIF1A WT and HIF1A del upregulated by hypoxia
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15843612

RA7EbrFjcEkmbDFRt5TwiVjvxzoVhN 0EwzgewyBrPJow
has assertion: p(HGNC:TP53,sub(Y,220,C)) =| tscript(p(HGNC:TP53))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.404+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

1
has substitution: Y,220,C
variant of: http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11998
type: http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00000

p(HGNC:TP53,sub(Y,220,C)) =| tscript(p(HGNC:TP53))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845392

5
value: From mutations file
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845392

RAwFQSXCO31Pr8jdn3BhdujKMK6eosXNMW1j0kZrEJ0VM
has assertion: path(SDIS:"blood flow") -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.405+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"blood flow") -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845398

2
value: Glucose uptake into various tissues has been reported to be enhanced by insulin-mediated vasodilation and the decrease in local blood flow to lead to the development of insulin resistance [1] and [2].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845398

RA3Ob6-G7s9dZDNiZzE8-s0DG2KC-VNMxlHEQVm tKrUM
has assertion: bp(GO:"response to hypoxia") -| r(HGNC:PPARG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.407+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| r(HGNC:PPARG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845540

3
value: Both hypoxia-mimetic deferoxamine mesylate (DFO) and TGF-beta1 inhibited adipocyte differentiation (1.0% versus the control at 15 microm DFO and 1.4% versus the control at 1 ng/ml TGF-beta1) and adipocyte gene expression (peroxisome proliferator-activated receptor-gamma2 and lipoprotein lipase) in human MSCs after 21 days of treatment. Hypoxia (2% O(2)) and DFO (but not TGF-beta1) increased hypoxia-inducible factor-1alpha as shown by Western blotting.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845540

RA5TUChOEcPsu QihOJB8vTgPdx7i1hE28oBXk7zm5LIs
has assertion: a(CHEBI:progesterone) -> r(MGI:Ckmt1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.416+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Ckmt1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 3. The list of uterine genes significantly increased and decreased by acute P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA9-MVVleAhmtJncI6p6moMlKjuOaguHsIiVNcEMOVrVo
has assertion: a(CHEBI:progesterone) -> r(MGI:Enpp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.417+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Enpp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 3. The list of uterine genes significantly increased and decreased by acute P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA9Qxyy fQVXEtJvIpdBggXF2OW-EYgIqOALHuLkYVMTE
has assertion: a(CHEBI:progesterone) -> r(MGI:G6pdx)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.418+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:G6pdx)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 3. The list of uterine genes significantly increased and decreased by acute P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA3v9-MSXLtIYGF2dMH5Q6WqBm3SMwC6H3xT2mP92gy9E
has assertion: a(CHEBI:progesterone) -> r(MGI:Ncaph)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.428+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Ncaph)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 3. The list of uterine genes significantly increased and decreased by acute P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA2amsJdE3Di970J1wjkWw7n1U0InFTsNrR MQgMp8tRE
has assertion: a(CHEBI:progesterone) -> r(MGI:Zdhhc3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.435+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Zdhhc3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 3. The list of uterine genes significantly increased and decreased by acute P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA5ML5BGT8ub-5uSm0eqXGiXRshhic Lp6v7ZOhN0HU0A
has assertion: a(CHEBI:progesterone) -> r(MGI:Basp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.439+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Basp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 4. The list of genes significantly increased and decreased uterine genes by chronic P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA-6acNFkzlaz0y5XHbZqMlkoEWIGbvV9Ar Ma2KTd35Q
has assertion: a(CHEBI:progesterone) -> r(MGI:Calb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.440+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Calb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 4. The list of genes significantly increased and decreased uterine genes by chronic P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAyQR1qyWzRHc8StcONhityWkH8VRIsomG8rRGjaiAIZg
has assertion: a(CHEBI:progesterone) -> r(MGI:Fam65b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.445+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Fam65b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 4. The list of genes significantly increased and decreased uterine genes by chronic P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAzf91zwUQWjGONJy6GVYade4R77RQ0va8PJG7rMYh85A
has assertion: a(CHEBI:progesterone) -> r(MGI:Hoxa10)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.447+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Hoxa10)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 4. The list of genes significantly increased and decreased uterine genes by chronic P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA jlQr4TWB03nmGAdHsa0lH6VVqIVCt7kvJeTNClFJj8
has assertion: a(CHEBI:progesterone) -> r(MGI:Rbp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.452+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Rbp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: TABLE 4. The list of genes significantly increased and decreased uterine genes by chronic P4 treatment upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAzgiSLPNyC3xgj D4V-0zFJCUo5lEY4Izi787B1mhMIE
has assertion: a(CHEBI:progesterone) -| r(MGI:Adipoq)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.456+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Adipoq)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA4GY0 -wtHLKZT24cePnP-S3AeReoyrPEoJLvX7EaZbM
has assertion: a(CHEBI:progesterone) -| r(MGI:Car3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.462+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Car3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAzDm4z4WIfSCg1qrrVNgDpxBaZzd6jIqvpqYZw-u9Ad4
has assertion: a(CHEBI:progesterone) -| r(MGI:Cebpb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.463+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Cebpb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAwJ FnI2xdApVo98Yxm8PXE0N0SyLt sLp7VNQ105rHU
has assertion: a(CHEBI:progesterone) -| r(MGI:Cp)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.465+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Cp)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA2HYaVs0MurY HSS7VSfGZwQofoV XDK6gdW9Ojoa5jc
has assertion: a(CHEBI:progesterone) -| r(MGI:Cd1d1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.470+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Cd1d1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAytnGPohlpZLXEK6C1u6w0d 0V2kxlOk6m5fWqIHzQEQ
has assertion: a(CHEBI:progesterone) -| r(MGI:Efna1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.474+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Efna1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA4NS4e51963K5ykUFif6Bs0CLWcTTXYY2OpEvwWUubys
has assertion: a(CHEBI:progesterone) -| r(MGI:Efnb2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.475+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Efnb2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA YTM4QqYaK6PPb86ZSZxA N8MZhyM3UDLZpRSVFPUHo
has assertion: a(CHEBI:progesterone) -| r(MGI:Emb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.476+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Emb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA9INYn8yKYp8S7wH8sx0LVQSaa0T8QecgmLNWS07bVAY
has assertion: a(CHEBI:progesterone) -| r(MGI:Fam3c)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.481+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Fam3c)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA-4C0o6jXKusUDs1Gx1rMWaMMsu64ID6wUfXK9DNe4-E
has assertion: a(CHEBI:progesterone) -| r(MGI:Gpam)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.486+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Gpam)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA2oKyWAVO43 hr2R-8U6o0YalgYIMP84CitH dluFaaE
has assertion: a(CHEBI:progesterone) -| r(MGI:Krt7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.492+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Krt7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA4-shapuxGGTVLIc 4SnGatAtYC3YmZnw9TZWfM A9wY
has assertion: a(CHEBI:progesterone) -| r(MGI:Lgr5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.493+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Lgr5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA9YoVAGGg 3YWGTlPpz4LGv dIhL786Y2w5s6cQNPTiM
has assertion: a(CHEBI:progesterone) -| r(MGI:Lpin1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.495+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Lpin1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA3k4GFmgZwAwSHyhEFFNGIAAt1g7ejnjXt793ak20X6Y
has assertion: a(CHEBI:progesterone) -| r(MGI:Ltf)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.496+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Ltf)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA4WhuDt4eG8TZ77VaErB5x1q24RRgWAWjXFlcuMfX12o
has assertion: a(CHEBI:progesterone) -| r(MGI:Scd1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.510+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Scd1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RA5zWvuT93sXjtG6sZKaiwZaORBN2sHND7WrSD8trIhwA
has assertion: a(CHEBI:progesterone) -| r(MGI:Tgfbi)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.516+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| r(MGI:Tgfbi)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15845616

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15845616

RAwONL BPESzFYkhe4zeBAh mvNXrhICjqFKapaCKRDac
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:ADH4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.534+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:ADH4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA4GysxZDJXLQfIurNumSx9a5q rR3c6VlC H8WB7KAl8
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:ERG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.542+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:ERG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RAyDHK3I0Ughlj9RoK8rv 53wtG yy5Y4X5QjE4N6UVs8
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:MAPK12)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.548+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:MAPK12)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RAyCHR3kD2wvntD57IABC6F7fnv3nhktgvxRdM5N7z61I
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:PPP1R13L)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.555+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:PPP1R13L)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA7L4krJ7Hg8xfdo6VvVSvs2HJ3CDnlrjjgxM0iKtmag0
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:STK17B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.561+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:STK17B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA1upckSEQeI5uzlUo4mm Sgmq2nIt6Yp7GCTOzblsvkc
has assertion: tscript(p(HGNC:HOXA9)) -> r(HGNC:TLX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.562+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -> r(HGNC:TLX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: Table 2. HOXA10-modulated genes in human CD34+ cord blood cells upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RAzf4eiiweIDqs-PaokPqN2RX IlE-YgvFhtbkRrIx20
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:BCL7A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.616+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:BCL7A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA5W4EhuyFUjc8VHZ8HfNv04LVMeaUibxrIJKf0wkAROc
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:HBE1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.631+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:HBE1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RAz62a1AsOxWBJ2QJxq60J4PwtKfLxepwike2pSijZVjE
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:HMBS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.638+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:HMBS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA6GXDBmQ1futg3PAepVDX0IhgszMFEh4LubIAWYTjmjA
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:KRT18)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.644+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:KRT18)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA7WNoRU9sh0871JEwHQuU9tXYlOZf20 fIAjveaWy8k4
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:MEIS2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.651+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:MEIS2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA75PAODlIYlQRv1h6Y16ipKvFfS6GH6ZBCt0cQR7eiZA
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:P4HB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.654+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:P4HB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA78bpKgqcGgeG0cai-Msqc35chgyO6eUlWgvH3WRGFsk
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:RPP40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.665+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:RPP40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RAx6PBDRE4080FtNDKbauNhw4YDkWu3LFo1X6WpIYAkKA
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:SNRPE)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.669+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:SNRPE)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA31Td3X2blPjqkuGr4RG94qyeBQnF878jgH2V-e4DUng
has assertion: tscript(p(HGNC:HOXA9)) -| r(HGNC:SAT1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.671+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HOXA9)) -| r(HGNC:SAT1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15849172

5
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15849172

RA7dWzpMiyhKQfeoti6OEPc0sTj6cLnWz2pby oPZ3Rlk
has assertion: a(CHEBI:"nitric oxide") -> r(HGNC:MAF)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.703+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"nitric oxide") -> r(HGNC:MAF)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15855057

3
value: Among the selected genes, 11 (ATF-4, c-maf, SGK-1, PBEF, ATPase 8, NADH dehydrogenase 4, STK6, TRAF4-associated factor 1, molybdopterin synthase, CKS1, and CIDE-B) have not been previously reported to be sensitive to ()NO.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15855057

RA1NjeAQxcNjZxXJUlZ9RSF7TputiWLH6E9UcNIv-5XEU
has assertion: a(CHEBI:"nitric oxide") -> r(HGNC:CDKN1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.720+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"nitric oxide") -> r(HGNC:CDKN1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15855057

3
value: PTIO-mediated increase in nitrosating species remarkably enhanced ()NO-dependent induction of IL-8, p21/Cip1, and MKP-1 and built a specific gene expression profile.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15855057

RA9MWhHW9NKtgfFVxMB0sUVHWh3h6Bq2VB5bwJ2P0zZxA
has assertion: gtp(p(PFH:"RAS Family")) -> r(HGNC:SPP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.732+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFH:"RAS Family")) -> r(HGNC:SPP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15857938

5
value: high levels of Bcr-Abl activate a signaling cascade involving the sequential activation of Ras, phosphatidylinositol-3 kinase, atypical protein kinase C, Raf-1, and mitogen-activated protein kinase kinase, leading to the ultimate expression of OPN.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15857938

RAxXXkZ0wuQSgzYlJZ8 3YOdhUWKQnABXLMtPjbJEyo44
has assertion: kin(p(HGNC:PRKCI)) -> kin(p(PFH:"MEK1/2 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.738+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKCI)) -> kin(p(PFH:"MEK1/2 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15857938

6
value: high levels of Bcr-Abl activate a signaling cascade involving the sequential activation of Ras, phosphatidylinositol-3 kinase, atypical protein kinase C, Raf-1, and mitogen-activated protein kinase kinase, leading to the ultimate expression of OPN.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15857938

RA8IPXMs4SWfFg9KTDUy9cBUKe9XZqmXOxKqgWeDxkI7g
has assertion: p(HGNC:EGF) => kin(p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.742+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) => kin(p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15858794

5
value: activation of EGF-R by EGF triggers signaling through the MAP kinase pathway during in vitro maturation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15858794

RA2LqwlVd Uyj5DmVmDUB5cwMCHPbck-v6ochSd52a0fM
has assertion: p(HGNC:TGFB1) -> cat(p(HGNC:DAXX))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.745+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFB1) -> cat(p(HGNC:DAXX))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15861194

5
value: Moreover, overexpressed Daxx positively modulates FAS-ligand and TGFbeta-induced apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15861194

RA18OsGnsvSyZ0K5fmQa5J 2kEfZ87vzVtmdJ7ZiiriS8
has assertion: p(HGNC:PLCG1,pmod(P,Y,783)) => cat(p(HGNC:PLCG1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.746+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PLCG1,pmod(P,Y,783)) => cat(p(HGNC:PLCG1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863030

5
value: PLC gamma is phosphorylated by activated FGFR, resulting in PLC gamma activation, stimulation of phosphatidyl inositol hydrolysis and generation of two second messengers, diacylglycerol and inositol (1,4,5) P3. Tyrosine phosphorylation of PLCgamma by FGFR4 is weaker than that seen by other isoforms of FGFR.Three tyrosine residues in PLC gamma have been identified as sites of receptor tyrosine kinase phosphorylation. Mutagenesis indicates that the phosphorylation at Tyr 783 is essential for IP3 formation, phosphorylation of Tyr 771 is dispensable, and phosphorylation of Tyr 1254 is necessary to achieve maximal IP3 formation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863030

RAzkv7GOrOd4zSIqj6Byg2FoZIcL2ILeToat9S5JDLCDM
has assertion: kin(p(HGNC:FGFR1)) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.750+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FGFR1)) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: Activation of FGFR1 or FGFR2 by angiogenic FGFs (including FGF1, FGF2, and FGF4) leads to endothelial cell proliferation [16].Recently, also the FGF8b isoform has been shown to stimulate endothelial cell proliferation in vitro [17].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RAwWu ZbpUqIDNrmZ1wdI-QJsBhtZ1KPLMVLPJlBEUbwM
has assertion: kin(p(HGNC:FGFR2)) -> bp(GO:angiogenesis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.751+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FGFR2)) -> bp(GO:angiogenesis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: Activation of FGFR1 or FGFR2 by angiogenic FGFs (including FGF1, FGF2, and FGF4) leads to endothelial cell proliferation [16].Recently, also the FGF8b isoform has been shown to stimulate endothelial cell proliferation in vitro [17].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA0x99Cxh4WPTmDDm2wtUlRxfINKYRVdQ0iIPDjLmOfy4
has assertion: p(HGNC:FGF2) -> p(HGNC:SERPINE1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.754+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FGF2) -> p(HGNC:SERPINE1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: Also, FGFs modulate the expression of uPA receptor on the endothelial cell surface, thus allowing the localization of the proteolytic activity at the leading edge of the cell at the front of migration [22]. Furthermore, FGF1 and FGF2 induce the expression of the plasminogen activator inhibitor (PAI)-1 in cultured endothelial cells leading to a fine modulation of the proteolytic balance [23-25].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RAyPNFzLUkINO-TOa69hsM2LX sfGesdOkTaohdOwNbE8
has assertion: p(HGNC:FGF2) -> p(HGNC:TIMP2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.770+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FGF2) -> p(HGNC:TIMP2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: FGF2 [50] and FGF8b [17] can enhance endothelial cell reorganization onMatrigel.The process requires the activation of the proteolytic machinery, including type IV collagenase(s) and TIMPs production [51] as well as uPA and PAI-1 upregulation [52], a6b1 integrin receptor engagement [53], PECAM-1 [54], and activation of the small GTPase Rac [55].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA1a13xlLncXSMsvShb6d-HbcWRMITSiZxzMsBBpwWW6A
has assertion: complex(a(CHEBI:ganglioside),p(HGNC:FGF1)) =| p(HGNC:FGF1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.779+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(a(CHEBI:ganglioside),p(HGNC:FGF1)) =| p(HGNC:FGF1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

5
value: Gangliosides bind FGF1, FGF2, and FGF4 via negatively charged Neu-Ac residues [147,148]. In the extracellular environment, gangliosides compete with free heparin for the binding to the growth factor. On endothelial cells, free gangliosides prevent the binding of FGF2 to FGFRs and HSPGs, thus inhibiting FGF2-mediated cell proliferation [147]. Ganglioside GM1 is expressed on the endothelial cell surface and binds FGF2 with an affinity that is significantly higher than that of its free counterpart (Table 1). Under these conditions, GM1 acts as a functional FGF2 co-receptor.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA9ob2zaXmzB9Xt06T00vEJ37mqMzzZe80sKLlNO Yq6Q
has assertion: complex(a(CHEBI:ganglioside),p(HGNC:FGF2)) =| p(HGNC:FGF2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.782+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(a(CHEBI:ganglioside),p(HGNC:FGF2)) =| p(HGNC:FGF2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

5
value: Gangliosides bind FGF1, FGF2, and FGF4 via negatively charged Neu-Ac residues [147,148]. In the extracellular environment, gangliosides compete with free heparin for the binding to the growth factor. On endothelial cells, free gangliosides prevent the binding of FGF2 to FGFRs and HSPGs, thus inhibiting FGF2-mediated cell proliferation [147]. Ganglioside GM1 is expressed on the endothelial cell surface and binds FGF2 with an affinity that is significantly higher than that of its free counterpart (Table 1). Under these conditions, GM1 acts as a functional FGF2 co-receptor.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA1OBuuBySV Y3xaCFi1ZDt6nQqzh7UsSLk1VI9WoWzBI
has assertion: complex(p(HGNC:SDC2),p(HGNC:FGF7)) => p(HGNC:FGF7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.792+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:SDC2),p(HGNC:FGF7)) => p(HGNC:FGF7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

6
value: In general, free heparin/HSPGs sequester FGFs in the extracellular environment and act as FGF antagonists. On the contrary, cellassociated HSPGs can directly activate a signal transduction pathway in response to FGF2 [124], promote FGF2 internalization [125,126], and are required for a correct presentation of FGFs to FGFRs, leading to the formation of productive HSPGs/FGF/FGFR ternary complexes [121].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RAyu5o3qz7n3DQrIX4EbiHZa2cJQCB1N6t0tpbPAj5bXE
has assertion: bp(GO:"inflammatory response") -> bp(GO:angiogenesis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.795+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"inflammatory response") -> bp(GO:angiogenesis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

2
value: Inflammation may promote FGF-dependent angiogenesis (Fig. 4). Inflammatory cells, including mononuclear phagocytes [204,205], CD4+ and CD8+ T lymphocytes [206,207], and mast cells [208] can express FGF2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA5WnbiaXwvysEE60mXJy2ZT-zy2R5aL-X0m8POfOe1uk
has assertion: cat(complex(p(HGNC:ITGAV),p(HGNC:ITGB3))) -> bp(GO:"cell migration")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.796+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(complex(p(HGNC:ITGAV),p(HGNC:ITGB3))) -> bp(GO:"cell migration")
label: p(HGNC:FGF2) -> (cat(complex(p(HGNC:ITGAV),p(HGNC:ITGB3))) -> bp(GO:"cell migration"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

8
value: Moreover, FGF2-mediated chemotaxis on fibronectincoated substrata can be attenuated by avb3 integrin inhibitors [34].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RAyGZKaZLM7H5 NRh0z4ES-U7yXx6HJ58E33LNkggJN9w
has assertion: cat(complex(p(HGNC:ITGAV),p(HGNC:ITGB3))) -> bp(GO:"cell migration")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.798+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(complex(p(HGNC:ITGAV),p(HGNC:ITGB3))) -> bp(GO:"cell migration")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

6
value: Moreover, FGF2-mediated chemotaxis on fibronectincoated substrata can be attenuated by avb3 integrin inhibitors [34].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA8bruKvUxXSGTZIlzR-h8RPnjAsiLPvx-qnXio8XxcV8
has assertion: bp(GO:"response to osmotic stress") -> p(HGNC:FGF2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.800+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to osmotic stress") -> p(HGNC:FGF2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

3
value: Moreover, osmotic shock and shear stress induce the release of FGF2 from endothelial cells [209,210]. FGF2 production and release from endothelial cells are also triggered by IFN-a plus IL-2 [211], IL-1b [212], and nitric oxide (NO) [213].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA1JGtOKeXOytlOzabNMc0sIE eiWQ2j 0sG7DoquhLbY
has assertion: p(HGNC:TNF) -> p(HGNC:PTX3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.804+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:PTX3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: On the other hand, PTX3, synthesized locally by endothelial cells in response to IL-1b and TNF-a, binds FGF2 and acts as a natural angiogenesis inhibitor (see above), thus allowing a fine tuning of FGF2 pro-angiogenic activity in inflammation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA5lt7-GtmLvtWUrIpYz-BUdkpVlPaTy8uL9ept-ZYoxo
has assertion: complex(p(HGNC:PTX3),p(HGNC:FGF2)) =| p(HGNC:FGF2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.806+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PTX3),p(HGNC:FGF2)) =| p(HGNC:FGF2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

6
value: PTX3 binds FGF2, but not FGF1 and FGF4, with high affinity [166]. In endothelial cells, PTX3 prevents the binding of FGF2 to cell surface FGFRs and HSPGs, with a consequent inhibition of cell proliferation and migration, and inhibits FGF2-dependent neovascularization in the CAM assay.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA3PLV4o1H717G5zjCnmGBqR7ORDlY2qWztYiN3EmXke4
has assertion: kin(p(HGNC:FGFR2)) -> p(HGNC:VEGFA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.812+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FGFR2)) -> p(HGNC:VEGFA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

5
value: Several experimental evidences point to the possibility that FGF2 induces neovascularization indirectly by activation of the VEGF/ VEGFR system. Indeed: (i) VEGFR-2 antagonists inhibit both VEGF and FGF2-induced angiogenesis in vitro and in vivo [98]; (ii) expression of dominant-negative FGFR1 or FGFR2 in glioma cells results in a decrease in tumor vascularization paralleled by VEGF down-regulation [99]; (iii) both endogenous and exogenous FGF2 modulate VEGF expression in endothelial cells [82]; (iv) in the mouse cornea, the quiescent endothelium of vessels of the limbus express both VEGF mRNA and protein only after FGF2 treatment. In the same model, systemic administration of anti-VEGF-A neutralizing antibodies dramatically reduces FGF2-induced vascularization [82]; (v) VEGFR-1-blocking antibodies or the expression of a dominant-negative VEGFR-1 result in a significant reduction of FGF2-induced cell extensions and capillary morphogenesis [56]; (vi) FGF2 upregulates the expression of both FGFRs and VEGFRs in endothelial cells [100].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA4d35qOOVW aEnSpcqBa1UffVp0A-wmB04Q-Pa8twXSY
has assertion: p(HGNC:FGF2) -> p(HGNC:TIMP2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.822+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FGF2) -> p(HGNC:TIMP2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863032

4
value: Stimulation of endothelial cells by FGF2 causes also the shedding of cell surface membrane vesicles containing MMP-2 and MMP-9 together with the two MMP inhibitors TIMP-1 and TIMP-2. These vesicles stimulate capillary-like structure formation when added to endothelial cells seeded on a solubilized basement membrane preparation (Matrigel) [26].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863032

RA26 cJ 22lKk 2-PhtA1TTaJbQ44foKXLEKaTrkyvJic
has assertion: kin(p(HGNC:ERBB4)) => p(HGNC:STAT5A,pmod(P,S,779))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.836+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ERBB4)) => p(HGNC:STAT5A,pmod(P,S,779))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863494

5
value: Here we show that STAT5A regulation by ERBB4 is also mediated through STAT5A serine phosphorylation. Using a reverse-phase high performance liquid chromatography tandem mass spectrometry analysis of proteolytically digested STAT5A coexpressed with ERBB4, we identified STAT5A serine phosphorylations at the previously described Ser-779 and at the novel Ser-127/Ser-128. Immunohistochemistry of wild-type and ERBB4-null mammary glands at late pregnancy showed that ERBB4 expression was required for STAT5A phosphorylation at Ser-779.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863494

RAwJ IqtI-5vZJREmtqbcjfXdCfAIBcQjULFah17zrUzU
has assertion: p(MGI:Sox15) -> r(MGI:Otx2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.841+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox15) -> r(MGI:Otx2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15863505

4
value: However, the expression of Otx2 (37), Ctgf (38), and Ebaf (39) were significantly decreased, whereas Hrc (40) was increased in Sox15-null ES cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15863505

RA6R5Ob y1O64BFDzlCOqXHHo78tYn1upYaHjruWZFFGI
has assertion: p(HGNC:PLCG1,pmod(P,Y,771)) => cat(p(HGNC:PLCG1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.849+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PLCG1,pmod(P,Y,771)) => cat(p(HGNC:PLCG1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

5
value: Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RA1Ac6ZToUrYvXaOgHROnuhiJRM-FqBbn8Bb6G9Gi9iL0
has assertion: kin(p(HGNC:EGFR)) => p(HGNC:PLCG1,pmod(P,Y,771))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.859+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) => p(HGNC:PLCG1,pmod(P,Y,771))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

5
value: Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RAxj0bbzVKk4g-SwxWCqdW-XkuVhE-MATnu 6rDntymKs
has assertion: p(HGNC:EREG) => complex(p(HGNC:ERBB4),p(HGNC:ERBB2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.861+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EREG) => complex(p(HGNC:ERBB4),p(HGNC:ERBB2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

6
value: Figure 1 | ERBB receptors, ligands, dimers and downstream signalling pathways. a | Members of the epidermal growth factor (EGF) family of growth factors are ligands for the ERBB receptors. Ligand binding to ERBB receptors induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues within the cytoplasmic tail. These phosphorylated residues serve as docking sites for a range of proteins, the recruitment of which leads to the activation of intracellular signalling pathways. None of the ligands bind ERBB2, but ERBB2 is the preferred dimerization partner for all the other ERBB receptors. ERBB3 has impaired kinase activity and only acquires signalling potential when it is dimerized with another ERBB receptor, such as ERBB2. Overexpression of ERBB2 in tumours leads to constitutive activation of ERBB2, presumably because of increased receptor concentrations at the plasma membrane. Many of these tumours contain phosphorylated ERBB3, which couples ERBB2 to the phosphatidylinositol 3-kinase (PI3K)?AKT pathway128.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RA6eyCN48k98rA7E8QFk1BuFDjY1m3H4fQmp9YxZK4y9Q
has assertion: p(HGNC:NRG1) => complex(p(HGNC:ERBB3),p(HGNC:ERBB2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.866+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NRG1) => complex(p(HGNC:ERBB3),p(HGNC:ERBB2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

6
value: Figure 1 | ERBB receptors, ligands, dimers and downstream signalling pathways. a | Members of the epidermal growth factor (EGF) family of growth factors are ligands for the ERBB receptors. Ligand binding to ERBB receptors induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues within the cytoplasmic tail. These phosphorylated residues serve as docking sites for a range of proteins, the recruitment of which leads to the activation of intracellular signalling pathways. None of the ligands bind ERBB2, but ERBB2 is the preferred dimerization partner for all the other ERBB receptors. ERBB3 has impaired kinase activity and only acquires signalling potential when it is dimerized with another ERBB receptor, such as ERBB2. Overexpression of ERBB2 in tumours leads to constitutive activation of ERBB2, presumably because of increased receptor concentrations at the plasma membrane. Many of these tumours contain phosphorylated ERBB3, which couples ERBB2 to the phosphatidylinositol 3-kinase (PI3K)?AKT pathway128.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RAyiOoFl0TTg4nGI1Vh8QdAB5QD0g ZlPUlhzlfBPnGJw
has assertion: p(HGNC:TGFA) => complex(p(HGNC:EGFR),p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.870+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFA) => complex(p(HGNC:EGFR),p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

6
value: Figure 1 | ERBB receptors, ligands, dimers and downstream signalling pathways. a | Members of the epidermal growth factor (EGF) family of growth factors are ligands for the ERBB receptors. Ligand binding to ERBB receptors induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues within the cytoplasmic tail. These phosphorylated residues serve as docking sites for a range of proteins, the recruitment of which leads to the activation of intracellular signalling pathways. None of the ligands bind ERBB2, but ERBB2 is the preferred dimerization partner for all the other ERBB receptors. ERBB3 has impaired kinase activity and only acquires signalling potential when it is dimerized with another ERBB receptor, such as ERBB2. Overexpression of ERBB2 in tumours leads to constitutive activation of ERBB2, presumably because of increased receptor concentrations at the plasma membrane. Many of these tumours contain phosphorylated ERBB3, which couples ERBB2 to the phosphatidylinositol 3-kinase (PI3K)?AKT pathway128.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RAz5u8MKrJORSgvOMPSxbQ26lQSYQ832td1MamKWZj9ds
has assertion: complex(p(HGNC:EGFR),p(HGNC:ERBB2)) => kin(p(HGNC:ERBB2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.875+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:EGFR),p(HGNC:ERBB2)) => kin(p(HGNC:ERBB2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864276

7
value: Figure 1 | ERBB receptors, ligands, dimers and downstream signalling pathways. a | Members of the epidermal growth factor (EGF) family of growth factors are ligands for the ERBB receptors. Ligand binding to ERBB receptors induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues within the cytoplasmic tail. These phosphorylated residues serve as docking sites for a range of proteins, the recruitment of which leads to the activation of intracellular signalling pathways. None of the ligands bind ERBB2, but ERBB2 is the preferred dimerization partner for all the other ERBB receptors. ERBB3 has impaired kinase activity and only acquires signalling potential when it is dimerized with another ERBB receptor, such as ERBB2. Overexpression of ERBB2 in tumours leads to constitutive activation of ERBB2, presumably because of increased receptor concentrations at the plasma membrane. Many of these tumours contain phosphorylated ERBB3, which couples ERBB2 to the phosphatidylinositol 3-kinase (PI3K)?AKT pathway128.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864276

RA8GGF8B5CBskacNCfWw5PgHg6 ozMLDQ8tfSwsgzlxpY
has assertion: kin(p(HGNC:BUB1B)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.886+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:BUB1B)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA761mveaPps 3OhPEKT-kAruOwdm3ZiBhzjvj-Hab0-k
has assertion: kin(p(HGNC:CAMK1G)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.889+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:CAMK1G)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA43rUgsVfSsI27wMGEs7wGq3A9G cutrd-aTki7FDcRs
has assertion: kin(p(HGNC:CAMK2D)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:CAMK2D)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA8OXR6QTDMzVvNLdUu3ectMjlcTc9D9MTrEOj1lF7jeg
has assertion: kin(p(HGNC:CHKA)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.902+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:CHKA)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA1aLZbJdPcx5pD8ZpEpHDUyiAke2Ab rINXSpOfJ8mCI
has assertion: kin(p(HGNC:JAK1)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.911+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:JAK1)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA-NE MkKtS6Hi2thWRSMF2Jh6UcZ50BxVQt4GlK7KmBc
has assertion: kin(p(HGNC:NEK3)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.914+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:NEK3)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA4iQHSt0xWkouFK1C qmpBI7g1fQ4Umpf15Vczw8AE o
has assertion: kin(p(HGNC:PFKFB2)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.918+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PFKFB2)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA1-VBekdUlae5hPYimrXY24Yb6fpeB4EVnA9ZCICw-xU
has assertion: kin(p(HGNC:PRKCQ)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.923+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKCQ)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAwGtzekUiIS090XEmuNN8uTzZPr-DJaplfFqx5Ig5Aes
has assertion: kin(p(HGNC:RPS6KL1)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.929+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RPS6KL1)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA6GnhIwwmbGvuRyWdEkHAY8hujzzXIttDrUKt0X4FTpg
has assertion: kin(p(HGNC:TNK2)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.930+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:TNK2)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAyzAk02yDJ6lvry9ssaDk9k7cvaPtHkv3IALLmqKIl1s
has assertion: phos(p(HGNC:DUSP19)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.935+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:DUSP19)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA-PmBR8UwEpXJGf bxEQ-i881AHIUkf2iLNc6 M3r4lI
has assertion: phos(p(HGNC:G6PC)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.941+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:G6PC)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA8z-AnD0dNVJLS1fzqbHF6VSWpkulgSTy7vlk9GfJDRs
has assertion: phos(p(HGNC:PPP1R7)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.963+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PPP1R7)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAzRTMlWd8AJHc4EaL0rSj4j9aWhrbCiSdM9ZggoTQiWM
has assertion: phos(p(HGNC:PPP2CA)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.966+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PPP2CA)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAzbgsxTGXWkbcvmxR8x1RgrUSeGDGrYs70GC-UtG-s-U
has assertion: phos(p(HGNC:PPP2R3A)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.968+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PPP2R3A)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA8TRItS0Y6-f04Dc gAAoVgihbcFFBYmOzk4-5yD0zKg
has assertion: phos(p(HGNC:PPP2R4)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.969+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PPP2R4)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAxIf7ODk-xZuZsNZlE13WkxRJRm2lnmse7ES19ISnvs8
has assertion: phos(p(HGNC:PTPN5)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.978+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPN5)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAytzKTADxwUNAP7yoNU0lrPU5JY7hsPJPsWm4WHzK3so
has assertion: phos(p(HGNC:PTPRN2)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.982+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPRN2)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RAwwFkLMXWIaB3isEx-a3gkrpl9y4xt3C8IxzDk0O6ET4
has assertion: phos(p(HGNC:PTPRO)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.983+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPRO)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA10wdnWJ5vSjcVfm-Cm7C6kiaAWTcvbrdN2w0vlJ 5ZU
has assertion: phos(p(HGNC:SBF1)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.990+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:SBF1)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA-l3ygY4xcpNHwEd3dxOzJVNqwZ1AIUlljUpZxMI31Ik
has assertion: phos(p(HGNC:INPP5K)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.994+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:INPP5K)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864305

4
value: Evasion from apoptosis is a hallmark of cancer, and recent success using targeted therapeutics underscores the importance of identifying anti-apoptotic survival pathways. Here we utilize RNA interference (RNAi) to systematically screen the kinase and phosphatase component of the human genome.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864305

RA L0JvDRKE08Q7U7fAUvZ0EFV4BPIMn wfD1M90g3JDw
has assertion: tscript(p(HGNC:GCM1)) -> r(EGID:30816)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:34.995+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:GCM1)) -> r(EGID:30816)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864327

5
value: o biochemically characterize the transcriptional activity of GCMa/1, we set up an in vitro transcription system for human GCMa/1 (hGCMa/1). Using G-free reporter constructs carrying multiple copies of wild-type or mutant GCMa-binding site (GBS) in front of a synthetic TATA box, we observed specific transcriptional activities of recombinant hGCMa/1 proteins prepared from a baculovirus--insect cell or Escherichia coli expression system. We further characterized GCMa/1-mediated transcriptional activation on the native syncytin promoter. Using G-free reporter constructs containing the native syncytin promoter, a TATA box downstream of the proximal GBS in the syncytin promoter was shown to be essential for the transcription activation directed by hGCMa/1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864327

RA3ahd8jle3sg9dFOFcdoLf8gAQTsm ed9su9gXCFFa6w
has assertion: path(SDIS:"TLR signaling") -> kin(p(HGNC:IKBKB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.003+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"TLR signaling") -> kin(p(HGNC:IKBKB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: Again, the activation of these kinases in obesity highlights the overlap of metabolic and immune pathways; these are the same kinases, particularly IKK and JNK, that are activated in the innate immune response by Toll-like receptor (TLR) signaling in response to LPS, peptidoglycan, double-stranded RNA, and other microbial products
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RAwFL9JSDD4I9ji4dkmsZv7Siy2 mwhUwAJJ1ynolE9SI
has assertion: a(CHEBI:lipopolysaccharide) -> kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.004+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: Again, the activation of these kinases in obesity highlights the overlap of metabolic and immune pathways; these are the same kinases, particularly IKK and JNK, that are activated in the innate immune response by Toll-like receptor (TLR) signaling in response to LPS, peptidoglycan, double-stranded RNA, and other microbial products
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA8IGSARwLnKpdLmdS Z1q2anpTVrpH-DreE0cw3FvBMU
has assertion: bp(MESHPP:Obesity) positiveCorrelation kin(p(HGNC:PRKCQ))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.007+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation kin(p(HGNC:PRKCQ))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: Again, the activation of these kinases in obesity highlights the overlap of metabolic and immune pathways; these are the same kinases, particularly IKK and JNK, that are activated in the innate immune response by Toll-like receptor (TLR) signaling in response to LPS, peptidoglycan, double-stranded RNA, and other microbial products
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA7XGFxv-Cp57iDW9Ye7K87P7cM9aTqh-QU73ChxsN4xU
has assertion: a(SCHEM:"serum glucose") -> a(CHEBI:"reactive oxygen species")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.008+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum glucose") -> a(CHEBI:"reactive oxygen species")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

2
value: Due to increased delivery of glucose to adipose tissue, endothelial cells in the fat pad may take up increasing amounts of glucose through their constitutive glucose transporters. Increased glucose uptake by endothelial cells in hyperglycemic conditions causes excess production of ROS in mitochondria, which inflicts oxidative damage and activates inflammatory signaling cascades inside endothelial cells (101).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA-ecsN1gd2YFdOjcGHFCGoWOUO5ufpIV44fYgoZlZhKc
has assertion: bp(MESHPP:Obesity) positiveCorrelation kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.016+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: In obesity, JNK activity is elevated in liver, muscle, and fat tissues, and loss of JNK1 prevents the development of insulin resistance and diabetes in both genetic and dietary mouse models of obesity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RAyopz8Odj4QzCspt0paYWu23Sy4wZSXl8Z4LwrNpr93I
has assertion: p(HGNC:MYD88) -> path(MESHD:Atherosclerosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.022+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MYD88) -> path(MESHD:Atherosclerosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: Indeed, lack of MyD88, a critical mediator of TLR signaling, reduces atherosclerosis in apoE minus mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA023IkpDoggNCmlENdCa2Xm 3paKlhYF7lS0rYK5XY w
has assertion: a(CHEBI:"nitric oxide") -| bp(GO:"insulin receptor signaling pathway")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.044+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"nitric oxide") -| bp(GO:"insulin receptor signaling pathway")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

2
value: Overproduction of nitric oxide also appears to contribute to impairment of both muscle cell insulin action and beta cell function in obesity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA9IWl0U2 u-fhGXVgX7jELWFg61r04phatR79UBNovyE
has assertion: kin(p(HGNC:IKBKB)) -| bp(GO:"insulin receptor signaling pathway")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.046+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:IKBKB)) -| bp(GO:"insulin receptor signaling pathway")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: Several serine/threonine kinases are activated by inflammatory or stressful stimuli and contribute to inhibition of insulin signaling, including JNK, inhibitor of NF-kB kinase (IKK), and PKC-theta
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RAwbAHKv-esssjLObUQ-EEQSDTDSTaf6E99GJWqbNhlwA
has assertion: p(MGI:Hyou1) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.090+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Hyou1) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: Targeting of JNK using a synthetic inhibitor and/or an inhibitory peptide has been demonstrated to improve insulin action in obese mice and reduce atherosclerosis in the apoE-deficient rodent model (52, 53). These results directly demonstrate the therapeutic potential of JNK inhibitors in diabetes. TZDs, high-affinity ligands of PPARg, which are given clinically as insulin-sensitizing agents, likely improve insulin action through multiple mechanisms, including both activating lipid metabolism and reducing production of inflammatory mediators such as TNFalpha It has recently been demonstrated that mice in which the chaperone ORP150 is transgenically or adenovirally overexpressed exhibited reduced ER stress and improved insulin tolerance compared with controls, whereas reduction of the expression of this molecule in liver results in increased ER stress and insulin resistance
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA3pLiduWy1u6NXhppl0zkCb8JCG3D8Vi5AgFPoAo X2Y
has assertion: a(SCHEM:cytokine) -> kin(p(PFH:"MAPK JNK Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.095+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:cytokine) -> kin(p(PFH:"MAPK JNK Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

4
value: The 3 members of the JNK group of serine/threonine kinases, JNK-1, -2, and -3, JNK has recently emerged as a central metabolic regulator, playing an important role in the development of insulin resistance in obesity In response to stimuli such as ER stress, cytokines, and fatty acids, JNK is activated, whereupon it associates with and phosphorylates IRS-1 on Ser307, impairing insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA7Yg-W6Bobl7JIvOby8ojpXoKsZqgYAEgytrvgaeoNv4
has assertion: kin(p(PFH:"MAPK JNK Family")) -> p(HGNC:IRS1,pmod(P,S))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.098+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"MAPK JNK Family")) -> p(HGNC:IRS1,pmod(P,S))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

5
value: The 3 members of the JNK group of serine/threonine kinases, JNK-1, -2, and -3, JNK has recently emerged as a central metabolic regulator, playing an important role in the development of insulin resistance in obesity In response to stimuli such as ER stress, cytokines, and fatty acids, JNK is activated, whereupon it associates with and phosphorylates IRS-1 on Ser307, impairing insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA97o9CVZY0xA7M66lqom a1a-wDio9prP448Y EjiY8A
has assertion: p(HGNC:ADIPOQ) -> bp(GO:"fatty acid oxidation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.102+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ADIPOQ) -> bp(GO:"fatty acid oxidation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA9TJND2ZikXrK6XFgrpf417-Uv9VHZwmImtl89rIdxfI
has assertion: p(HGNC:IL10) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.107+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL10) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA3S89VOZz5OIdzne iAS-PFcyx3u0I6TBPdF GKVsorg
has assertion: p(HGNC:IL1R1) -| (p(HGNC:LEP) -| path(SDIS:"food intake"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.111+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL1R1) -| (p(HGNC:LEP) -| path(SDIS:"food intake"))
label: p(HGNC:LEP) -| path(SDIS:"food intake")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

5
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA5zAVxhW2ykrQY76cWmTeUFsRYfVKNwqEcNyir0CChCY
has assertion: p(HGNC:IL1R1) -| (p(HGNC:LEP) -> bp(GO:"fatty acid oxidation"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.113+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL1R1) -| (p(HGNC:LEP) -> bp(GO:"fatty acid oxidation"))
label: p(HGNC:LEP) -> bp(GO:"fatty acid oxidation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

5
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA74YsZiRI1sKZ95PwHPwSzKj506GjkbhoZ8he qMv9iE
has assertion: p(HGNC:IL6) -> bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.114+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL6) -> bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA23pLH5nppIr4QIEeQcKVVmWYZgONT5NulWDIY9ykUuw
has assertion: p(HGNC:MIF) -| bp(GO:"cell migration")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.120+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MIF) -| bp(GO:"cell migration")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RAxPm46wGWLqw3B6ExMGa7PFl8ZkP-cmYpYg4sQ3v0Pq0
has assertion: bp(GO:"inflammatory response") -> p(HGNC:RETN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.122+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"inflammatory response") -> p(HGNC:RETN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA3j6O1yNrsVVI87O bM27kZwNXBqO08fTkGBU7ahSZLY
has assertion: bp(MESHPP:Obesity) positiveCorrelation p(HGNC:CCL2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.125+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation p(HGNC:CCL2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA1UasXDiG59sj01KbgFSngnxXSXtDHmNlIrRCWH1wkME
has assertion: bp(MESHPP:Obesity) positiveCorrelation p(HGNC:IL6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.130+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation p(HGNC:IL6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RAwfjTdwMEUdK7ol42Q0c0IKI7-QyCGyO2ptKuzIiOBP0
has assertion: a(SCHEM:"serum glucose") -> p(HGNC:IL1B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.139+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum glucose") -> p(HGNC:IL1B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

3
value: This phosphorylation reduces both tyrosine phosphorylation of IRS-1 in response to insulin and the ability of IRS-1 to associate with the insulin receptor and thereby inhibits downstream signaling and insulin action
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA6xZQ9jgBNLgkZNm2qRwumSc0hImsiz3HVzp8zQ9DDbU
has assertion: bp(GO:"inflammatory response") -> bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.142+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"inflammatory response") -> bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15864338

2
value: even in the absence of obesity, infusion of animals with inflammatory cytokines or lipids can cause insulin resistance
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15864338

RA0IB20x-khsSOPK1dUMW Hhj8auxMMDCBhnid5mtIRO8
has assertion: phos(p(HGNC:PTPN1)) => kin(p(HGNC:SRC))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.148+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPN1)) => kin(p(HGNC:SRC))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15866871

6
value: These results establish that PTP1B promotes integrin-mediated responses in fibroblasts by dephosphorylating the inhibitory pTyr(527) and thereby activating the Src kinase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15866871

RA3vocsuq4Dc7a7JIrlkXLz2YwLC-QqOIK-MOW99j7ZrI
has assertion: phos(p(HGNC:PTPN1)) -> p(HGNC:MAPK1,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.150+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPN1)) -> p(HGNC:MAPK1,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15866871

5
value: We show that down-regulation of PTP1B activity with small molecule inhibitors suppresses cell spreading and migration to fibronectin, increases Tyr(527) phosphorylation in Src, and decreases phosphorylation of FAK, p130(Cas), and ERK1/2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15866871

RA1BpiI gWkf3tlNEex2n6 7i7Rcq2BkEkoSop7u6bmcI
has assertion: kin(p(HGNC:GSK3B)) => p(HGNC:LGALS3,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.152+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:GSK3B)) => p(HGNC:LGALS3,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15867344

5
value: Analysis of the human gal-3 sequence reveled a structural similarity to beta-catenin as it also contains the consensus sequence (S92XXXS96) for glycogen synthase kinase-3beta (GSK-3beta) phosphorylation and can serve as its substrate.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15867344

RA0BwqoYc4TZuBn2YA92RJK0GLO0aYusHUWotn0jHo1xk
has assertion: a(SCHEM:Progestins) -> cat(p(HGNC:FASN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.174+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Progestins) -> cat(p(HGNC:FASN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15870863

4
value: We found that in estrogen receptor (ER)- and progesterone receptor (PR)-positive MCF-7 human breast cancer cells, synthetic progestins used in oral contraceptives including norethynodrel (NOR) and norethindrone, induced a dose-dependent increase of FAS enzymatic activity, with a maximum response (> or = 4-fold) occurring at a concentration of 10(-8) M. FAS activity was only slightly stimulated after exposure to two other progestins, medroxy-progesterone acetate (MPA) and megestrol acetate (MGA), which are used in postmenopausal hormone replacement therapy and high-dose progestin treatment therapy. Western blot analyses showed that NOR-induced stimulation of FAS activity correlated closely with NOR-induced up-regulation of FAS protein expression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15870863

RA fsEb4Zq2xEB6vyZTJtDBCgleTAVNass3yPEH9Y3Xc
has assertion: p(MGI:Vegfa) -> tscript(p(PFM:"Notch Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.180+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Vegfa) -> tscript(p(PFM:"Notch Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15875024

5
value: The current model of arterial-venous identity proposes that binding of vascular endothelial growth factor to its heterodimeric receptor--Flk1 and neuropilin 1 (NP-1; also called Nrp1)--activates the Notch signalling pathway in the endothelium, causing induction of ephrin B2 expression and suppression of ephrin receptor B4 expression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15875024

RAwKyBetMf94cGg7 iTKWkT7sZ hU6PehBqOrLvtStEoY
has assertion: cat(p(MGI:Vegfa)) -> tscript(p(PFM:"Notch Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.182+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Vegfa)) -> tscript(p(PFM:"Notch Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15875024

6
value: The current model of arterial-venous identity proposes that binding of vascular endothelial growth factor to its heterodimeric receptor--Flk1 and neuropilin 1 (NP-1; also called Nrp1)--activates the Notch signalling pathway in the endothelium, causing induction of ephrin B2 expression and suppression of ephrin receptor B4 expression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15875024

RA5yC15eTuNO6Et2zWTbxyj6plXHHuECZ3NTNurc2n-Vg
has assertion: tscript(p(PFM:"Notch Family")) -> r(MGI:Efnb2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.184+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(PFM:"Notch Family")) -> r(MGI:Efnb2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15875024

5
value: The current model of arterial-venous identity proposes that binding of vascular endothelial growth factor to its heterodimeric receptor--Flk1 and neuropilin 1 (NP-1; also called Nrp1)--activates the Notch signalling pathway in the endothelium, causing induction of ephrin B2 expression and suppression of ephrin receptor B4 expression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15875024

RA60YPr J6Ty GWmZrkFKLzYMQOCD9P38wjApVvwKlq8I
has assertion: cat(p(HGNC:HSD11B1)) -> tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.187+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:HSD11B1)) -> tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15877012

6
value: 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) locally regenerates active cortisol from inactive cortisone amplifying glucocorticoid receptor activation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15877012

RA AMzsDnsI-ZpfSue0nCaOu3aOFVuzQxa7HmUi3fr8P4
has assertion: a(CHEBI:testosterone) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.192+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:testosterone) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15877079

2
value: These data show that Par4 has an important role in tumour suppression, with a particular relevance in the endometrium and prostate.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15877079

RA8LxO78sg10h5JT0B0BrkK7Mp4IwDrtvOpfBmXTVhhEM
has assertion: cat(p(RGD:Alox15)) -| kin(p(RGD:Pdgfrb))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.200+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Alox15)) -| kin(p(RGD:Pdgfrb))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15878884

6
value: Conversely, the receptors for transforming growth factor-beta and platelet-derived growth factor, which contributed to down-regulation of sPLA2-IIA expression, were decreased following 12/15-LOX overexpression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15878884

RA3sslxmTC5Ti-KcGXruW6193118Lty8xtCPecSvK0CrU
has assertion: cat(p(RGD:Alox12)) -| kin(p(RGD:Pdgfrb))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.203+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Alox12)) -| kin(p(RGD:Pdgfrb))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15878884

6
value: Conversely, the receptors for transforming growth factor-beta and platelet-derived growth factor, which contributed to down-regulation of sPLA2-IIA expression, were decreased following 12/15-LOX overexpression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15878884

RA-tLueynmZORMIkf85CAqthf5JJL3GNOEniMG9sFswXk
has assertion: complex(p(HGNC:CYTH3),p(HGNC:THRA)) =| tscript(p(HGNC:THRA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.206+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:CYTH3),p(HGNC:THRA)) =| tscript(p(HGNC:THRA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15878955

7
value: Thyroid hormone receptors (TRs) bind to response elements (TREs) located in the promoter region of target genes and modulate their transcription. We reconfirmed the interaction between TRs and GRP1 in yeast and glutathione-S-transferase pull-down assays, and determined the areas of TRs and GRP1 involved in the interaction. Coimmunoprecipitation studies demonstrated that the interaction between GRP1 and TRs takes place in the cytoplasm and the nucleus of mammalian cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15878955

RA7aj lUCLGx1IIdVfVXRkFAoiHerkvGO4W39DZIb3yCI
has assertion: p(HGNC:CYTH3) =| tscript(p(HGNC:THRA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.207+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CYTH3) =| tscript(p(HGNC:THRA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15878955

5
value: addition of GRP1 diminishes the formation of TR/TR homodimers and TR/retinoid X receptor heterodimers on TREs, which could explain the effect of GRP1 on transcription.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15878955

RA5AXH1WWm-cf5qiYs5ScrXu ULFIOLHM0VpJZ-6YAUy8
has assertion: p(MGI:Ifng) -> p(MGI:Cebpb,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.213+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Ifng) -> p(MGI:Cebpb,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15879117

4
value: In response to IFN-gamma, C/EBP-beta undergoes phosphorylation at a critical ERK1/2 phosphorylation motif.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15879117

RA1zmwyl-IQ-RMVavLUgxrDJTFrOvTE7o3RBoXPoA7qRw
has assertion: p(HGNC:TNF) -> cat(p(HGNC:FAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> cat(p(HGNC:FAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15879156

5
value: Apart from counteracting matrix metalloproteinases, tissue inhibitor of metalloproteinases-3 (TIMP-3) has proapoptotic properties.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15879156

RA66xLfOm3WzywvWL9Ez17fhFiARD2LTw2vnUOkN0QAYU
has assertion: a(CHEBI:progesterone) -> r(MGI:Tsc22d1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.220+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Tsc22d1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15881652

3
value: tsc-22 mRNA is expressed in almost all organs of mice and humans and its expression is induced in a variety of cell lines by many different factors including TGF-beta, phorbol ester, serum, and progestin
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15881652

RAzrnh1RzzeUf0fAN3zGikM8-cljLcWDXJE3XSYtP8v Q
has assertion: gtp(p(MGI:Cdc42)) -> bp(GO:"nuclear migration")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.223+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(MGI:Cdc42)) -> bp(GO:"nuclear migration")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15882626

4
value: By direct imaging of wound-edge fibroblasts after triggering MTOC reorientation with soluble factors, we found instead that the nucleus moved away from the leading edge to reorient the MTOC, while the MTOC remained stationary. Rearward nuclear movement was coupled with actin retrograde flow and was regulated by a pathway involving Cdc42, MRCK, myosin, and actin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15882626

RAxVbfPjfc13cxCbNV4-W-7DhqMGIV-b8QTVQZ8c8WvSU
has assertion: bp(GO:"response to radiation") -> tloc(p(HGNC:ITGA6),GOCCACC:"GO:0005886",GOCCACC:"GO:0005622")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.231+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to radiation") -> tloc(p(HGNC:ITGA6),GOCCACC:"GO:0005886",GOCCACC:"GO:0005622")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15885076

4
value: By immunofluorescence, we could demonstrate that UVB leads to a dose-dependent internalization of alpha6-integrin
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15885076

RAzWslN4THWLUZwFnczBRRUqI-ayyqDEpw2iGV8oD7X44
has assertion: bp(GO:"response to radiation") -| surf(p(HGNC:ITGA6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.232+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to radiation") -| surf(p(HGNC:ITGA6))
label: complex(NCH:"Laminin 1 Complex") -| (bp(GO:"response to radiation") -| surf(p(HGNC:ITGA6)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15885076

5
value: In the presence of LM-1, the UVB-induced down-regulation of alpha6-integrin in melanocytes was significantly reduced
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15885076

RA95jSYqS6uK7Yyrz Fq3aRcGKQWl-FJShl CR1FxrWjg
has assertion: bp(GO:"response to radiation") -| surf(p(HGNC:ITGA6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.234+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to radiation") -| surf(p(HGNC:ITGA6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15885076

4
value: We were able to demonstrate that the alpha6-integrin subunit is selectively and reversibly down-regulated by UVB
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15885076

RAy6km5AItqijAyr9WiRJW-Kipo5QurheQZzJFf0N5y2A
has assertion: p(HGNC:WNT3A) -> complex(p(HGNC:RHOA),p(HGNC:DVL2),p(HGNC:DVL3),p(HGNC:PRKCA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.248+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:WNT3A) -> complex(p(HGNC:RHOA),p(HGNC:DVL2),p(HGNC:DVL3),p(HGNC:PRKCA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15886323

8
value: PKCa, PCKb, and PKCmu were associated with both Dvl-2 (Figure 8A) and Dvl-3 (Figure 8B), suggesting that several PKCs are likely included in the Dvl/RhoA complex.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15886323

RA2UIMCA7OVjWS-XmMkxKW0StPr3ncTJJGxifD8AN-qFY
has assertion: p(HGNC:PLAUR) -> path(SDIS:metastasis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.254+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PLAUR) -> path(SDIS:metastasis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15886816

3
value: (1) the levels of Her2, but not of EGFR, as well as the uPA secretion, cell motility and Matrigel invasion were statistically higher in AR negative than in AR positive PCa cells;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15886816

RA8X7VqSxCeyWBPQIv6rjcP28F jTdMr3s9H85icXNQ-w
has assertion: p(HGNC:EGF) -> bp(GO:"cell motility")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.259+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> bp(GO:"cell motility")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15886816

3
value: (2) the uPA secretion and uPA Rexpression were positively related to Matrigel invasion; (3) the EGF was able to stimulate chemotaxis and Matrigel invasion in a dose-dependent manner;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15886816

RA0qQHgWyI0T3gnUopRYmQ uTnoXWdRw2XyolG2gp34gs
has assertion: complex(p(HGNC:PLAU),p(HGNC:PLAUR)) => cat(p(HGNC:PLAU))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.263+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PLAU),p(HGNC:PLAUR)) => cat(p(HGNC:PLAU))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15886816

7
value: (4) the EGF-induced cell migration was statistically higher inAR negative than in AR positive cells with a similar increase with respect to basal value (about 2.6 fold); (5) the Matrigel invasion was statistically higher in AR negative than in AR positive PCa cells also if the increment of Matrigel invasion after EGF treatment was statistically higher in AR positive respect to AR negative cells; (6) the EGF induced uPA secretion and its membrane uptake through the increment of uPAR;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15886816

RA6HtEfpf1JurNYvgWSIyssoCIYBRtneO-6JlnZ99YXzc
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:metastasis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.265+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:metastasis)
label: phos(p(HGNC:PTEN)) -| (kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:metastasis))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15886816

6
value: (7) these effects were blocked by EGFR/Her2 tyrosine kinase inhibitors with IC(50) lower than those needed to inhibit cell proliferation and required PI3K/Akt, MAPK and PI-PLC activities as verified by inhibition experiments. inhibition of PI3K blocked the EGF-induced invasiveness in PTEN positive cells but not in PTEN negative cells,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15886816

RA9CGjVwGbEWcKcQoAsCW351nvC7BUZ-j WSHupTru3jU
has assertion: a(CHEBI:wortmannin) -| (p(EGID:183) -> cat(complex(NCH:"Na/K Exchanging ATPase Complex")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.271+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:wortmannin) -| (p(EGID:183) -> cat(complex(NCH:"Na/K Exchanging ATPase Complex")))
label: p(EGID:183) -> cat(complex(NCH:"Na/K Exchanging ATPase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15887250

5
value: The treatment of cells with PKC-iota antisense oligodeoxynucleotides inhibited the effects of Ang II on the Na+/K+ATPase activity. Additionally, the effect of Ang II on Na+/K+ATPase activity was also blocked by the phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002, and by the actin depolymerizing agents, cytochalasin D.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15887250

RAxu6LBAXFaJJOEHVmkcxRyUVEWFFpYeFHGdvTIORTe I
has assertion: p(EGID:183) -> cat(complex(NCH:"Na/K Exchanging ATPase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.276+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:183) -> cat(complex(NCH:"Na/K Exchanging ATPase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15887250

4
value: We demonstrated previously that in serum-starved MCF-7 breast cancer cell line, Ang II increased Na+/K+ATPase activity and activated the protein kinase C zeta (PKC-zeta) (Muscella et al., 2002 J Endocrinol 173:315-323; 2003 J Cell Physiol 197:61-68.).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15887250

RA W3KQHPS9T4kMtxyUC2efoSGC19YvCoFtGVc4pFgS5I
has assertion: p(HGNC:EGF) -> kin(p(HGNC:MAPK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.280+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> kin(p(HGNC:MAPK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888452

5
value: We show that Cdc2 inhibits EGF-mediated ERK activation through direct interaction and phosphorylation of several ERK pathway proteins, including the guanine nucleotide exchange factor, Sos-1, and Raf-1 kinase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888452

RA7c0aXNi046-5BNjKirlBMw0mZT8SUtGxY2airZQnzOI
has assertion: kin(p(EGID:5424)) -| (p(HGNC:EGF) -> kin(p(HGNC:MAPK1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.283+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(EGID:5424)) -| (p(HGNC:EGF) -> kin(p(HGNC:MAPK1)))
label: p(HGNC:EGF) -> kin(p(HGNC:MAPK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888452

8
value: We show that Cdc2 inhibits EGF-mediated ERK activation through direct interaction and phosphorylation of several ERK pathway proteins, including the guanine nucleotide exchange factor, Sos-1, and Raf-1 kinase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888452

RA9PPu AZEb6uYdH17k-bIiXKMvfSBzGijCMFZzng61Vw
has assertion: kin(p(EGID:5424)) -| kin(p(HGNC:RAF1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.284+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(EGID:5424)) -| kin(p(HGNC:RAF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888452

6
value: We show that Cdc2 inhibits EGF-mediated ERK activation through direct interaction and phosphorylation of several ERK pathway proteins, including the guanine nucleotide exchange factor, Sos-1, and Raf-1 kinase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888452

RA4SyTItveyNhNqnFgzVdDywAczvhFkJKtq zGM3Nmug8
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Idh2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.293+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Idh2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA4YZny7kuL9xes f-YoiOVKIofow5T22S-Hiyz2VGHyY
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Rxrg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.302+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Rxrg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA-g1svMDnQj81LOMlPEXhk7CbX5e84AeyejXmNVcDdT0
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Retn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.303+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Retn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA1RjgC2eehIPc4 bgcUWKQp9aesBfGtrXWzzd9T0G5PM
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Pfkfb3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.306+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -| r(MGI:Pfkfb3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA8rbS1 wYcwlV5uVLum5PtohH53whStAkf7K-siI-MII
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Cpt1a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.310+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Cpt1a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA3cBxeRYalWQItaiE28tCGJY0XTdr0W-Y2jpbIrAnwO8
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Gpam)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.312+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Gpam)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA8VBWxZYgFhDm56mi76sXBDQI7rOkHU9Yk 1xLc51wiE
has assertion: a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Slc25a20)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.319+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"trans10,cis12-Octadecadienoate") -> r(MGI:Slc25a20)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15888570

3
value: Gene expression was measured during t10c12-CLA-induced body fat reduction in a polygenic obese line of mice. Adult mice (n = 185) were allotted to a 2 x 2 factorial experiment consisting of either nonobese (ICR-control) or obese (M16-selected) mice fed a 7% fat, purified diet containing either 1% linoleic acid (LA) or 1% t10c12-CLA. Body weight (BW) by day 14 was 12% lower in CLA- compared with LA-fed mice (P of epididymal, mesenteric, and brown adipose tissues, as a percentage of BW, in both lines by 30, 27, and 58%, respectively, and increased liver weight/BW by 34% (P per day) from epididymal adipose (days 5 and 14) of the obese mice to analyze gene expression profiles using Agilent mouse oligo microarray slides representing 20,000 genes. Numbers of genes differentially expressed by greater than or equal to twofold in epididymal adipose (days 5 and 14) were 29 and 125, respectively. It was concluded that, in adipose tissue, CLA increased expression of uncoupling proteins (1 and 2), carnitine palmitoyltransferase system, tumor necrosis factor-alpha (P caspase-3 but decreased expression of peroxisome proliferator-activated receptor-gamma, glucose transporter-4, perilipin, caveolin-1, adiponectin, resistin, and Bcl-2 (P candidate genes that will be useful in elucidating mechanisms of adipose delipidation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15888570

RA OIFkry8rdCc4lJcWOqSb7ACxUNLNPjfh0QICq2CGKg
has assertion: a(SCHEM:Oxidopamine) -> r(HGNC:DDIT3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.327+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Oxidopamine) -> r(HGNC:DDIT3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890008

3
value: Notably, stress-induced transcription factors such as ATF3, ATF4, CHOP, and C/EBP beta were robustly up-regulated, yet exhibited unique kinetic patterns. Genes involved in the synthesis and modification of proteins (various tRNA synthetases), protein degradation (e.g., ubiquitin, Herpud1, Sqstm1), and oxidative stress (Hmox1, Por) could be subgrouped into distinct kinetic profiles as well.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890008

RA-zIg yfEEGsmpB1E2DnjLVxXOwOT-ihnSA -VjItb E
has assertion: a(SCHEM:Oxidopamine) -> r(HGNC:HERPUD1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.329+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Oxidopamine) -> r(HGNC:HERPUD1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890008

3
value: Notably, stress-induced transcription factors such as ATF3, ATF4, CHOP, and C/EBP beta were robustly up-regulated, yet exhibited unique kinetic patterns. Genes involved in the synthesis and modification of proteins (various tRNA synthetases), protein degradation (e.g., ubiquitin, Herpud1, Sqstm1), and oxidative stress (Hmox1, Por) could be subgrouped into distinct kinetic profiles as well.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890008

RA0arKlJpbHDrRktp3Qz1cdm8YuoLY6wAfdGgGmbqvuI8
has assertion: p(HGNC:AKT2,pmod(P,T,309)) => kin(p(HGNC:AKT2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.340+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AKT2,pmod(P,T,309)) => kin(p(HGNC:AKT2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890450

5
value: Upon stimulation with insulin, AKT is recruited to cellular membranes by binding of its amino terminal pleckstrin (PH) domain to membrane bound phosphatidylinositol 3,4,5, trisphosphate (PIP3) [3]. The membrane bound form of AKT then becomes phosphorylated on two regulatory residues, a threonine within the activation loop (Thr308 in AKT1,Thr309 in AKT2, Thr305 in AKT3) and a serine in the C-terminus of the enzyme (Ser473 in AKT1,Ser474 in AKT2, Ser472 in AKT3), and both phosphorylations are considered to be required for AKT to reach maximum kinase activity [1]. The kinase responsible for phosphorylation of Thr308/309/305 has been identified as phosphoinositide-dependent kinase 1 (PDK1) [3].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890450

RA4hWc0dfkfEumf6Vb6OL 96lNCnaWSHWIzcH5AHKiFZE
has assertion: cat(p(MGI:Prdx6)) -| bp(GO:"response to oxidative stress")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.348+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Prdx6)) -| bp(GO:"response to oxidative stress")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890616

4
value: Prdx6 stably overexpressed in cells protected against oxidative stress, whereas antisense treatment resulted in oxidant stress
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890616

RA3mOhPHSRMN71mVJ8eL DRBysKed0T-CRuZh7bp-VrCA
has assertion: kin(p(HGNC:MAPK1)) => p(HGNC:CAD,pmod(P,T,456))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.349+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK1)) => p(HGNC:CAD,pmod(P,T,456))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890648

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890648

RA4iytZSEy91GjL ooZAnYMhbxvVriagOzmoEDULPluc0
has assertion: kin(p(HGNC:MAPK3)) => p(HGNC:CAD,pmod(P,T,456))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.351+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) => p(HGNC:CAD,pmod(P,T,456))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890648

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890648

RAxb7a2xYyWfIDVV-ZPyktTgzarLs4HO307Lu95ZKAFIQ
has assertion: p(MGI:Calm1) -> kin(p(MGI:Raf1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.357+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Calm1) -> kin(p(MGI:Raf1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890671

5
value: GnRH-induced phosphorylation of MAPK/ERK kinase 1 and c-Raf kinase was blocked by Cam inhibition
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890671

RA501uoYLlLDPLl687C3DVyk-IA96RMeGxEVEbpN7GkgE
has assertion: p(MGI:Map2k1,pmod(P)) => kin(p(MGI:Map2k1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.359+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Map2k1,pmod(P)) => kin(p(MGI:Map2k1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890671

5
value: GnRH-induced phosphorylation of MAPK/ERK kinase 1 and c-Raf kinase was blocked by Cam inhibition
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890671

RAxkEIzfZfxtMCqFFd7swCPHyt5VqP7bENfzPy9sX3qJY
has assertion: gtp(p(HGNC:CDC42)) => cat(p(HGNC:IQGAP1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.364+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:CDC42)) => cat(p(HGNC:IQGAP1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15890984

6
value: Activated Rac1 and Cdc42 form a tripartite complex with IQGAP1 and APC (Watanabe et al., 2004). The depletion of IQGAP1 or APC by RNAi inhibits formation of an actin meshwork at the leading edge, as well as cell migration, immobilization of the plus-ends of microtubules and polarization of the MTOC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15890984

RA8OeYA-ViOWB62Jg0eyqxi Z7fv50qEiHdAtTCFTQ5iI
has assertion: tscript(p(MGI:Foxo3)) -| r(MGI:Fasl)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.372+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo3)) -| r(MGI:Fasl)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15895074

5
value: This reflects a need for Foxo3a to maintain neutrophil vitality during inflammation by suppressing Fas ligand; because Foxo3a can bind and suppress the Fasl promoter,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15895074

RA18S7WKeD78fWnqFsqD71y255IuKBncTJXh20LFWUgCo
has assertion: p(HGNC:APOE) -| path(SDIS:"LDL oxidation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.373+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:APOE) -| path(SDIS:"LDL oxidation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15896001

3
value: Taken together, these results localized the antioxidant domain of apoE to its receptor binding domain and the basic amino acids in this domain are important for its antioxidant activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15896001

RAwvmYvy7GvEzGieAevMg8J1L x M-tqh8I2UXggagt3U
has assertion: p(HGNC:APOE) -| a(CHEBI:"reactive oxygen species")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.375+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:APOE) -| a(CHEBI:"reactive oxygen species")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15896001

3
value: Taken together, these results localized the antioxidant domain of apoE to its receptor binding domain and the basic amino acids in this domain are important for its antioxidant activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15896001

RA pjOeRmCtD 4CK8pAgR gzZPNOddmfbu6 U0II3IOEI
has assertion: phos(p(HGNC:PTPRF)) -> kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.380+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPRF)) -> kin(p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15896785

6
value: Knock-down of LAR induced post-receptor insulin resistance with the insulin-induced activation of PKB/Akt and MAP kinases markedly inhibited.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15896785

RA eOQnm2nV5pR9ec HDjQ4JaCK j2HS-4t-5CadoYllw
has assertion: cat(p(HGNC:ADIPOR2)) -> tscript(p(HGNC:PPARA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.385+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:ADIPOR2)) -> tscript(p(HGNC:PPARA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15897298

6
value: We showed that AdipoR1 and AdipoR2 serve as receptors for globular and full-length adiponectin and mediate increased AMP-activated protein kinase, peroxisome proliferator-activated receptor-alpha ligand activities, and glucose uptake and fatty-acid oxidation by adiponectin
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15897298

RA9WuXibnx2jqu-jPdiqEfeNPu8dRBVBeSu2K7EZCUs4A
has assertion: p(HGNC:ING4) -| tscript(p(HGNC:HIF1A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.386+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ING4) -| tscript(p(HGNC:HIF1A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15897452

5
value: suppression of ING4 further induces HIF transcriptional activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15897452

RA9fDPjpmEPWjw-zAsR05VsPwMZc4nCxZnrQ1JPUnGAeo
has assertion: a(CHEBI:calcitriol) -| r(MGI:Agtr1a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.388+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -| r(MGI:Agtr1a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15897475

3
value: In the presence of cortisone (1 to 10 nM), there was significant cortisol production, which was dose dependently augmented (2- to 6-fold, p 0.001) by 1,25-dihydroxyvitamin D3 (0.1 to 10 nM). 1,25-Dihydroxyvitamin D3 dose dependently increased 11beta-HSD 1 expression up to 2-fold (p 0.01) in both the presence and absence of cortisone. In contrast, 1,25-dihydroxyvitamin D3 dose dependently decreased adipocyte AT1 expression (by 30% to 50%, p 0.001) in both the presence and absence of cortisone, suggesting compensatory down-regulation of AT(1)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15897475

RAzvotkyBCpvM0P5-LOMNOzpmXptyBjYYS9Pf4Pep8AFU
has assertion: a(CHEBI:calcitriol) -> a(SCHEM:Hydrocortisone)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.389+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -> a(SCHEM:Hydrocortisone)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15897475

2
value: In the presence of cortisone (1 to 10 nM), there was significant cortisol production, which was dose dependently augmented (2- to 6-fold, p 0.001) by 1,25-dihydroxyvitamin D3 (0.1 to 10 nM). 1,25-Dihydroxyvitamin D3 dose dependently increased 11beta-HSD 1 expression up to 2-fold (p 0.01) in both the presence and absence of cortisone. In contrast, 1,25-dihydroxyvitamin D3 dose dependently decreased adipocyte AT1 expression (by 30% to 50%, p 0.001) in both the presence and absence of cortisone, suggesting compensatory down-regulation of AT(1)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15897475

RAz94AvnztAaSx xKLC 4afr1b5jGfinRHj-zvMQQ4FbU
has assertion: bp(MESHPP:Obesity) negativeCorrelation phos(p(EGID:54704))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.393+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) negativeCorrelation phos(p(EGID:54704))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15897476

4
value: At T0 in ObS, PDHt was normal, whereas PDHa and PDP1 activity was below normal at all Mg/Ca concentrations.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15897476

RA9ETVt2PjgAUq oLwl7R5i-xuuIVlUc36daq9udWWcd8
has assertion: a(CHEBI:"trichostatin A") -| r(HGNC:ADAMTS9)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.404+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"trichostatin A") -| r(HGNC:ADAMTS9)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899037

3
value: The HDAC inhibitors trichostatin A and sodium butyrate potently inhibit cartilage degradation in an explant assay. These compounds decrease the level of collagenolytic enzymes in explant-conditioned culture medium and also the activation of these enzymes. In cell culture, these effects are explained by the ability of HDAC inhibitors to block the induction of key MMPs (e.g. MMP-1 and MMP-13) by proinflammatory cytokines at both the mRNA and protein levels. The induction of aggrecan-degrading enzymes (e.g. ADAMTS4, ADAMTS5, and ADAMTS9) is also inhibited at the mRNA level.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899037

RA7SNK0pNjspt1FOfqUuCyqh37CLe3eQ-YX4CuSc0sYn0
has assertion: a(CHEBI:"trichostatin A") -| r(HGNC:MMP13)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.408+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"trichostatin A") -| r(HGNC:MMP13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899037

3
value: The HDAC inhibitors trichostatin A and sodium butyrate potently inhibit cartilage degradation in an explant assay. These compounds decrease the level of collagenolytic enzymes in explant-conditioned culture medium and also the activation of these enzymes. In cell culture, these effects are explained by the ability of HDAC inhibitors to block the induction of key MMPs (e.g. MMP-1 and MMP-13) by proinflammatory cytokines at both the mRNA and protein levels. The induction of aggrecan-degrading enzymes (e.g. ADAMTS4, ADAMTS5, and ADAMTS9) is also inhibited at the mRNA level.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899037

RA9qIcTBm5JvKeYKi85AUUFMmLIN5vWojbA8LUB1epGUs
has assertion: p(HGNC:COPS5) -| p(HGNC:ESR1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.412+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:COPS5) -| p(HGNC:ESR1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899841

4
value: Here, we show that estrogen receptor alpha (ERalpha) coimmunoprecipitates with CSN5/Jab1, a subunit of the COP9 signalosome (CSN), and that overexpression of CSN5/Jab1 causes an increase in ligand-induced ERalpha degradation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899841

RA6Cr1sDCyV6LGI65hy-ymOuCVoGeMHfaPlGzU8UsMF2s
has assertion: p(MGI:Raf1,pmod(P,S,43)) =| kin(p(MGI:Raf1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.417+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Raf1,pmod(P,S,43)) =| kin(p(MGI:Raf1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899852

5
value: Phosphorylation at Raf-1 S43 and S259 by PKA only weakly inhibited EGF activation of Raf-1 and ERK when cells maintained high Raf-1 S338 phosphorylation. Raf-1 inhibition in suspension was not due to excessive negative regulation on inhibitory sites S43 and S259, as these serines were largely dephosphorylated in suspended cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899852

RA-XGKpEwSnkfOJRnYXlfWGoAMJ3-xf-HniF- 8ea qX0
has assertion: p(MGI:Raf1,pmod(P,S,338)) -> kin(p(MGI:Mapk1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.419+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Raf1,pmod(P,S,338)) -> kin(p(MGI:Mapk1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899852

5
value: Restoration of phosphorylation at S338, either by expression of highly active PAK or by expression of an S338 phospho-mimetic Raf-1 mutation, led to a partial rescue of ERK activation in suspended cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899852

RA tGmBLgaG kwHJdwSYL5UonnPPrSTgaOqbjPQdx06LA
has assertion: p(MGI:Raf1,pmod(P,S,338)) -> kin(p(MGI:Mapk3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.420+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Raf1,pmod(P,S,338)) -> kin(p(MGI:Mapk3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899852

5
value: Restoration of phosphorylation at S338, either by expression of highly active PAK or by expression of an S338 phospho-mimetic Raf-1 mutation, led to a partial rescue of ERK activation in suspended cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899852

RA7HC7xoJvR-964dqFABFPYKCnhihBSLAGN RxXqvAcFU
has assertion: kin(p(MGI:Pak1)) -> kin(p(MGI:Mapk1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.422+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Pak1)) -> kin(p(MGI:Mapk1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899852

6
value: Restoration of phosphorylation at S338, either by expression of highly active PAK or by expression of an S338 phospho-mimetic Raf-1 mutation, led to a partial rescue of ERK activation in suspended cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899852

RA1Aibq B4OaC2A13g1zBJuTRavW2twEf3lPpRgSX-gZs
has assertion: p(MGI:Tnf) -> complex(p(MGI:Bid),p(MGI:Mtch2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.427+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Tnf) -> complex(p(MGI:Bid),p(MGI:Mtch2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899861

6
value: Activation of the TNF-R1 receptor results in the cleavage of BID into truncated BID (tBID), which translocates to the mitochondria and induces the activation of BAX or BAK. In TNF-alpha-activated FL5.12 cells, tBID becomes part of a 45-kDa cross-linkable mitochondrial complex. Here we describe the biochemical purification of this complex and the identification of mitochondrial carrier homolog 2 (Mtch2) as part of this complex.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899861

RA4SzD7E QDiuAMt36L873ZEy9FrBgZkYh5x7qQiF72j4
has assertion: p(HGNC:TNFRSF1B) -> kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.432+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNFRSF1B) -> kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15899873

5
value: ASB3 expression and activities are required for (i) TNF-R2 ubiquitination both in vivo and in vitro, (ii) TNF-R2 proteolysis via the proteasome pathway, and (iii) the inhibition of TNF-R2-mediated Jun N-terminal protein kinase (JNK) activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15899873

RA6AQMKi55R31FGUieJY-zMkMuitFQBHKZH-h1xN1aUCw
has assertion: complex(p(MGI:Prkcz),p(MGI:Pawr)) -| (kin(p(MGI:Prkcz)) -> tscript(complex(NCM:"Nfkb Complex")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.450+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Prkcz),p(MGI:Pawr)) -| (kin(p(MGI:Prkcz)) -> tscript(complex(NCM:"Nfkb Complex")))
label: kin(p(MGI:Prkcz)) -> tscript(complex(NCM:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15901738

9
value: A luciferase reporter assay showed that ceramide analogs activate nuclear factor (NF)-kappaB unless PAR-4-dependent inhibition of PKCzeta suppresses NF-kappaB activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15901738

RA8S9kk4PSuV7V1 y8dlyQ4f7THFl h-swBqZIVUyMahY
has assertion: a(CHEBI:ceramide) -> p(MGI:Prkcz,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.456+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ceramide) -> p(MGI:Prkcz,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15901738

3
value: Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15901738

RA-cQb49q8Edm3WFMVsRQBUKc6LLnZAlCMZPwQB8hjS4k
has assertion: complex(p(MGI:Prkcz),p(MGI:Pawr)) -| kin(p(MGI:Prkcz))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.467+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Prkcz),p(MGI:Pawr)) -| kin(p(MGI:Prkcz))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15901738

7
value: We have reported that ceramide mediates binding of atypical protein kinase C (PKC) zeta to its inhibitor protein, PAR-4 (prostate apoptosis response-4), thereby inducing apoptosis in differentiating embryonic stem cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15901738

RA6mdzcW7UZ-UPNFJq182ZVyb YXp 1VUF 4nlcrG5LTY
has assertion: kin(p(PFH:"EGFR/ERBB Family")) -> tscript(p(HGNC:CREB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.472+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"EGFR/ERBB Family")) -> tscript(p(HGNC:CREB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15901830

6
value: Both in vitro and in vivo DNA binding assay revealed that the CREB binding activity was low in EGF-starved cells, whereas it was induced within 30 min after EGF treatment
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15901830

RA37 MSknrJY2hvAe1gzgYD9uRDnrs5NWRdqZI96bDGRE
has assertion: cat(p(HGNC:CXCR4)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.488+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:CXCR4)) -| bp(MESHPP:Apoptosis)
label: p(HGNC:CXCL12) -> (cat(p(HGNC:CXCR4)) -| bp(MESHPP:Apoptosis))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15905192

6
value: TC14012 and TN14003 antagonized the antiapoptotic effect of synthetic CXCL12 and stromal cell-mediated protection of CLL cells from spontaneous apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15905192

RA3MG18nNOkzm6w2touXV7dqwG zBiQAabRQLXhE0QFj0
has assertion: p(HGNC:LEP) -> p(HGNC:IL12A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.495+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:LEP) -> p(HGNC:IL12A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15905523

4
value: At a functional level, leptin up-regulates the IL-1beta, IL-6, IL-12, TNF-alpha, and MIP-1alpha production.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15905523

RA63sghm2f0zUf0AzouZwkMZeSjkoXB49WgaJDHtBX19o
has assertion: p(HGNC:LEP) -> complex(p(HGNC:IL12A),p(HGNC:IL12B))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.500+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:LEP) -> complex(p(HGNC:IL12A),p(HGNC:IL12B))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15905523

6
value: At a functional level, leptin up-regulates the IL-1beta, IL-6, IL-12, TNF-alpha, and MIP-1alpha production.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15905523

RA6tWeWMwLaIxzbPQqErhUW2Y5zI2RhyPCgB5MHeHH0EA
has assertion: bp(GO:"response to UV") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.511+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15905523

2
value: Finally, we found that leptin partly protects DCs from spontaneous and UVB-induced apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15905523

RA4woLlmsYFEvGgg2gTFxMd-eEfqno6Pa5Y8Fa5xuUaq8
has assertion: cat(p(HGNC:LEPR)) -| p(HGNC:IL10)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.515+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:LEPR)) -| p(HGNC:IL10)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15905523

5
value: Furthermore, we found that leptin down-regulates IL-10 production by DCs and drives naive T cell polarization toward Th1 phenotype.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15905523

RAweVpt ryivJNRWKhMw-3Q7IcBRrBzPjcyf-dFfAmHzY
has assertion: p(MGI:Prok1) -| p(MGI:Cxcr4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.521+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Prok1) -| p(MGI:Cxcr4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15908459

4
value: Expression of {Cell surface} CD14, B7-1, CCR5, and CXCR4 was down-regulated on PK1-treated monocytes when compared with monocytes treated with a control or Csf-1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15908459

RA FaKeDRfs7KvSmRPxf3cmverUy7lu-G885eelU 2phw
has assertion: kin(p(HGNC:MAP3K5)) => kin(p(HGNC:MAP2K4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.533+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K5)) => kin(p(HGNC:MAP2K4))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15911620

6
value: Glucose deprivation rapidly increases the interaction between ASK1 and JIP3, and the consequently activated ASK1 phosphorylates SEK1 on the Thr-261 residue.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15911620

RA7IYBDK9abSKW0IMIL9n siuJ0EhDc-LOMFwpm9digYM
has assertion: tscript(p(HGNC:PPARGC1A)) -> bp(GO:"regulation of membrane potential")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.536+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:PPARGC1A)) -> bp(GO:"regulation of membrane potential")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15914121

4
value: Endothelial cells that overexpress PGC-1alpha show reduced accumulation of reactive oxygen species (ROS), increased mitochondrial membrane potential, and reduced apoptotic cell death both in basal and oxidative stress conditions
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15914121

RA33pR-K1Q4f1wh8-NUKt59baL63lCZOOJsUfLMDETpV8
has assertion: p(HGNC:ALB) -> a(CHEBI:glutathione)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.540+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ALB) -> a(CHEBI:glutathione)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15915465

3
value: Furthermore, HSA augments intracellular glutathione levels and influences activation of the ubiquitous transcription factor nuclear factor-kappa B using both in vitro and in vivo protocols.32
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15915465

RA9tZKKoXuLqORki6Arv5v0joF5ZjXn2EYoxLR sxhWNI
has assertion: cat(p(HGNC:ADIPOQ)) -| (p(HGNC:TNF) -> path(SDIS:"monocyte adherence"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.549+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:ADIPOQ)) -| (p(HGNC:TNF) -> path(SDIS:"monocyte adherence"))
label: p(HGNC:TNF) -> path(SDIS:"monocyte adherence")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15916985

6
value: Adiponectin dose dependently suppresses TNF-A-stimulated adherence of monocytes to cultured human endothelial cells. This effect results from inhibition of the expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and intercellular adhesion molecule-1 (ICAM-1). TNF-A increases, whereas adiponectin reduces, the amount of these proteins and their respective mRNAs in endothelial cells [56].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15916985

RA NPY718jSOugCwmq9M1lGM6KSDzix8q-4SskhSXFfPw
has assertion: a(SCHEM:"serum insulin") -| r(MGI:Retn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.636+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -| r(MGI:Retn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15916985

3
value: Insulin down-regulated resistin expression in 3T3-L1 adipocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15916985

RA88ryVj3KYezu15d5CQWVK0BABzhggr0LVR7nW86SU 0
has assertion: a(SCHEM:"serum leptin") -> kin(p(PFR:"MAPK Erk1/3 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.640+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum leptin") -> kin(p(PFR:"MAPK Erk1/3 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15916985

4
value: Leptin administration to culture media to reach physiological and pathophysiologic concentrations dose-dependently increases both migration and proliferation of rat vascular smooth muscle cells [25] through activation of phosphatidylinositol-3-kinase and mitogen-activated protein kinases.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15916985

RA9cC7eHZ3jg43LWFVoL9yF0mG4zwONK21OUoLB0vWlKw
has assertion: a(SCHEM:"serum leptin") -> path(SDIS:"macrophage TNF secretion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.659+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum leptin") -> path(SDIS:"macrophage TNF secretion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15916985

2
value: in vitro administration of leptin to lipopolysaccharide (LPS)- activated macrophages collected from ob-/ob- and db-/db- mice substantially potentiates secretion of tumor necrosis factor and interleukins-2 and -6. These results indicate that leptin is involved in the regulation of immune function and cytokine secretion in ob/ob mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15916985

RA5EQmUHW2OAMZecF02GmKx4avPSs1pWtVNH0ddcEJLVc
has assertion: kin(p(HGNC:MAPK8)) => p(HGNC:FOXO4,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.691+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK8)) => p(HGNC:FOXO4,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15917664

5
value: JNK then phosphorylates cytoplasmic FOXO proteins at the C-terminal sites that are distinct from the Akt phosphorylation sites. JNK-induced phosphorylation initiates nuclear import of FOXO proteins and activation of their transcriptional regulatory potential.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15917664

RA5KZ3g1bJPFCyh3azy3CdSo36zzDIRunA ug6GlsHNUc
has assertion: gtp(p(HGNC:RALA)) -> kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.695+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:RALA)) -> kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15917664

6
value: Oxidative stress... leads to an activation of the small GTPase Ral, which in turn is instrumental in the phosphorylation and activation of the Jun N-terminal kinase JNK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15917664

RAwVRFJkmKyPMDDDIhBClzDFzrVd74LnlWqSc y0UcU9w
has assertion: tscript(p(HGNC:FOXO3)) => r(HGNC:CAT)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.709+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:FOXO3)) => r(HGNC:CAT)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15917664

5
value: Transcriptional control by FOXO also extends to the regulation of pro-apoptotic genes Bim and Fas Ligand and to the stress response genes like GADD45, Mn superoxide dismutase and catalase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15917664

RA575q2w5pcVQ0NBz3y5R7X4-XW KPbyRPCPFmtfOSTGc
has assertion: tscript(p(HGNC:FOXO4)) => r(HGNC:CAT)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.711+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:FOXO4)) => r(HGNC:CAT)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15917664

5
value: Transcriptional control by FOXO also extends to the regulation of pro-apoptotic genes Bim and Fas Ligand and to the stress response genes like GADD45, Mn superoxide dismutase and catalase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15917664

RA-w82J2FUVW6IGwmSnQr8GDTZZ1HyKqrH5ndGzE0336I
has assertion: a(CHEBI:glutathione) -| a(CHEBI:"reactive oxygen species")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.722+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:glutathione) -| a(CHEBI:"reactive oxygen species")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

2
value: In the process of reducing high intracellular glucose to sorbitol, the aldose reductase consumes the cofactor NADPH (6). But as shown in Fig. 2, NADPH is also the essential cofactor for regenerating a critical intracellular antioxidant, reduced glutathione. By reducing the amount of reduced glutathione, the polyol pathway increases susceptibility to intracellular oxidative stress.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RA-eSDl-sc-rywQJxaNfCvLmf9fT7B6IsQMh73gTYGAak
has assertion: a(SCHEM:"Advanced Glycation End Product") -> bp(GO:"inflammatory response")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Advanced Glycation End Product") -> bp(GO:"inflammatory response")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

2
value: The third mechanism, shown on the right of Fig. 3, is that these AGE precursors diffuse out of the cell and modify circulating proteins in the blood such as albumin. These modified circulating proteins can then bind to AGE receptors and activate them, thereby causing the production of inflammatory cytokines and growth factors,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RA7y1YI0AXCWzFHAwfXhxt1Ts7b9GV-Wp6uV0RAXxGh0k
has assertion: a(SCHEM:"D-Glucose, anhydrous") -> a(SCHEM:Diacylglycerol)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.729+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"D-Glucose, anhydrous") -> a(SCHEM:Diacylglycerol)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

2
value: hyperglycemia inside the cell increases the synthesis of a molecule called diacylglycerol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RA35DcNANB794ETOTmtGdXLECAN09QD-9fEIxRCgPJu0U
has assertion: kin(p(PFH:"PRKC Family")) -> r(HGNC:EDN1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.735+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKC Family")) -> r(HGNC:EDN1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

5
value: it has a variety of effects on gene expression, examples of which are shown in the row of open boxes in Fig. 4.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RA7bkH7h b3cPsYa5E36ioxvJnJBt9ws6liBju5VWg8ws
has assertion: kin(p(PFH:"PRKC Family")) -> r(HGNC:FN1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.738+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKC Family")) -> r(HGNC:FN1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

5
value: it has a variety of effects on gene expression, examples of which are shown in the row of open boxes in Fig. 4.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RAx0pN4YN4Oc fXdGIF0J4ubwvpSIF907ojRCZbgS1xvE
has assertion: a(SCHEM:Diacylglycerol) => kin(p(PFH:"PRKC Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.753+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Diacylglycerol) => kin(p(PFH:"PRKC Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919781

4
value: which is a critical activating cofactor for the classic isoforms of protein kinase-C, -beta, -delta, and -alpha
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919781

RA5YKlOhC5DwWSBlx0 xhKfOuhWBvdOxBDdwPia ebFSI
has assertion: a(CHEBI:spironolactone) -> tscript(p(MGI:Nr1i2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.767+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:spironolactone) -> tscript(p(MGI:Nr1i2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15919853

4
value: Two PXR ligands [pregnenolone-16alpha-carbonitrile (PCN) and spironolactone] increased Oatp1a4 mRNA expression in liver,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15919853

RA3-mpaPkvx3-4vPcRmKeEJ7rHIaWrza8comOA1f01218
has assertion: complex(p(HGNC:ARHGDIB),p(HGNC:CDC42)) =| gtp(p(HGNC:CDC42))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.769+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ARHGDIB),p(HGNC:CDC42)) =| gtp(p(HGNC:CDC42))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15921909

7
value: Both RhoGDI and D4GDI (hereafter referred to collectively as GDIs) are cytosolic and form 1:1 complexes with Rho family GTPases, although several Rho family members have been reported to not effectively bind to GDIs (Table 1). First, they inhibit the dissociation of GDP from Rho proteins, maintaining the GTPase in an inactive form and preventing GTPase activation by GEFs (Box 1). Second, they are able to interact with the GTP-bound form of the Rho GTPase to inhibit GTP hydrolysis, blocking both intrinsic and GAP-catalyzed GTPase activity and preventing interactions with effector targets.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15921909

RA-vaQBRlMB41sLqVqYYhRm3TDElncK3uxCNXvi7DjIh8
has assertion: complex(p(HGNC:ARHGDIB),p(HGNC:RAC1)) =| gtp(p(HGNC:RAC1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.771+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ARHGDIB),p(HGNC:RAC1)) =| gtp(p(HGNC:RAC1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15921909

7
value: Both RhoGDI and D4GDI (hereafter referred to collectively as GDIs) are cytosolic and form 1:1 complexes with Rho family GTPases, although several Rho family members have been reported to not effectively bind to GDIs (Table 1). First, they inhibit the dissociation of GDP from Rho proteins, maintaining the GTPase in an inactive form and preventing GTPase activation by GEFs (Box 1). Second, they are able to interact with the GTP-bound form of the Rho GTPase to inhibit GTP hydrolysis, blocking both intrinsic and GAP-catalyzed GTPase activity and preventing interactions with effector targets.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15921909

RA6M TV8VRpQnXghTtBXfbTt76VIgLYpEWb00mbPj2feQ
has assertion: p(HGNC:SNN) -| kin(p(PFH:"MAPK Erk1/3 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.778+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SNN) -| kin(p(PFH:"MAPK Erk1/3 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923056

5
value: In addition, we present the evidence that Snn overexpression results in reduced extracellular regulated kinase activation and increased p38 activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923056

RA4pInNHHO2rmFxLLfu1hjwMQUBulklMlbX3e4xPSu2pc
has assertion: bp(GO:"response to hypoxia") -> tscript(p(MGI:Hif1a))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.786+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> tscript(p(MGI:Hif1a))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923604

4
value: Here, we demonstrate that p38alpha-/- cells fail to activate HIF-1 under hypoxic conditions.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923604

RA38PJsJTY0zdWj5bpU-7givIP1-3L-9NbEGMRBqihrHs
has assertion: bp(GO:"response to hypoxia") -> tscript(p(MGI:Hif1a))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.787+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> tscript(p(MGI:Hif1a))
label: kin(p(MGI:Mapk14)) -> (bp(GO:"response to hypoxia") -> tscript(p(MGI:Hif1a)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923604

7
value: Here, we demonstrate that p38alpha-/- cells fail to activate HIF-1 under hypoxic conditions.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923604

RAzg0NXSgljWBx9QkgquplMEJLsvBV7uORA-d0d3gNB9U
has assertion: cat(p(MGI:G6pdx)) -> r(MGI:Cebpa)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.788+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:G6pdx)) -> r(MGI:Cebpa)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923630

5
value: As shown in Fig. 5F, the mRNA expression levels of most lipogenic genes including G6PD, 6PGD, ME, ADD1/SREBP1c, and FAS and those of adipogenic genes including PPARgamma, C/EBPalpha, and aP2 were greatly decreased in G6PD-11i-infected 3T3-L1 cells, indicating that a certain amount of G6PD appears to be required for the execution of both adipogenesis and lipogenesis in adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923630

RAxQFDPCNkvJeuwWYc4 ZWKmPi2m7PQYYj1f6UZolF3cU
has assertion: cat(p(MGI:G6pdx)) -> r(MGI:Fabp4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.790+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:G6pdx)) -> r(MGI:Fabp4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923630

5
value: As shown in Fig. 5F, the mRNA expression levels of most lipogenic genes including G6PD, 6PGD, ME, ADD1/SREBP1c, and FAS and those of adipogenic genes including PPARgamma, C/EBPalpha, and aP2 were greatly decreased in G6PD-11i-infected 3T3-L1 cells, indicating that a certain amount of G6PD appears to be required for the execution of both adipogenesis and lipogenesis in adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923630

RAyeu8ohwUhdM0BSE8jtpF8xGZxHxaRm7gGIv03FLLDnU
has assertion: cat(p(MGI:G6pdx)) -> r(MGI:Fasn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.791+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:G6pdx)) -> r(MGI:Fasn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923630

5
value: As shown in Fig. 5F, the mRNA expression levels of most lipogenic genes including G6PD, 6PGD, ME, ADD1/SREBP1c, and FAS and those of adipogenic genes including PPARgamma, C/EBPalpha, and aP2 were greatly decreased in G6PD-11i-infected 3T3-L1 cells, indicating that a certain amount of G6PD appears to be required for the execution of both adipogenesis and lipogenesis in adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923630

RA2HlhS7e4tUH502mPxGyGAgizo0MH-Vly5cRXHiWj Qg
has assertion: cat(p(MGI:G6pdx)) -> r(MGI:Pparg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.795+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:G6pdx)) -> r(MGI:Pparg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923630

5
value: As shown in Fig. 5F, the mRNA expression levels of most lipogenic genes including G6PD, 6PGD, ME, ADD1/SREBP1c, and FAS and those of adipogenic genes including PPARgamma, C/EBPalpha, and aP2 were greatly decreased in G6PD-11i-infected 3T3-L1 cells, indicating that a certain amount of G6PD appears to be required for the execution of both adipogenesis and lipogenesis in adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923630

RA5IsZDQmWlSSww5TPQN8iFFiEiYPRD 70cUadpOm0EEU
has assertion: cat(p(MGI:G6pdx)) -> r(MGI:Retn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.801+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:G6pdx)) -> r(MGI:Retn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15923630

5
value: Surprisingly, the expression of certain adipocytokines such as tumor necrosis factor alpha and resistin was increased, whereas that of adiponectin was decreased in G6PD overexpressed adipocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15923630

RA5wZw31B-9Coz5k8uuNCgHG9ZLNd7cluRxiyDPk4uk04
has assertion: tscript(p(HGNC:HMGA1)) -> surf(p(HGNC:INSR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.805+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HMGA1)) -> surf(p(HGNC:INSR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15924147

6
value: Lack of the architectural factor HMGA1 causes insulin resistance and diabetes in humans and mice Restoration of HMGA1 protein expression in subjects' cells enhanced INSR gene transcription, and restored cell-surface insulin receptor protein expression and insulin-binding capacity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15924147

RA2qN-Vkn25r5FqTetyrmXbYsPiKVnvWfwpg-IRl7KQJY
has assertion: tscript(p(MGI:Hmga1)) -> sec(a(SCHEM:"serum insulin"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.806+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Hmga1)) -> sec(a(SCHEM:"serum insulin"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15924147

5
value: Loss of Hmga1 expression, induced in mice by disrupting the Hmga1 gene, considerably decreased insulin receptor expression in the major targets of insulin action, largely impaired insulin signaling and severely reduced insulin secretion, causing a phenotype characteristic of human type 2 diabetes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15924147

RA7ns5cBGO0JLTrU 9oP6aWGj21CxKheFF8L7VcmQvbWA
has assertion: kin(p(HGNC:MAP3K5)) -> p(HGNC:PDCD6,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.808+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K5)) -> p(HGNC:PDCD6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15925322

5
value: We also found that apoptosis signal-regulating kinase 1 (ASK1) strongly phosphorylated ALG-2. Importantly, Raf-1 blocks the ASK1-dependent ALG-2 phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15925322

RA2aV aan275aeZezPL4lUwjF4LZVnLv5sES7my5aA2Aw
has assertion: p(MGI:Thbs1) -| bp(GO:"monocyte extravasation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.816+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Thbs1) -| bp(GO:"monocyte extravasation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15927970

3
value: TSP-1-/- mice had markedly increased macrophage and myofibroblast density
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15927970

RAw2zIc0yQipVe6YkuB0id5got6VCGj4vq66XoJJ9MMlw
has assertion: tscript(p(HGNC:TP53)) -| gtp(p(HGNC:HRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.818+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP53)) -| gtp(p(HGNC:HRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15930270

6
value: Supplementary Figure 3 Cluster of upregulated genes that correlate with INK4A locus [inactivation].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15930270

RA3NgURczrihzNKuWWo QHE0Y29Q8JdXt1I lW V-OeSY
has assertion: tscript(p(MGI:Cebpa)) -> bp(GO:"cell differentiation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.837+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Cebpa)) -> bp(GO:"cell differentiation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15936931

4
value: The first transcription factors found to participate in adipogenesis were members of the bZIP family of CCAAT/enhancer binding proteins (C/EBPs), specifically C/EBPa, C/EBPb, and C/EBPd. Upon the addition of adipogenic cocktail to 3T3-L1 pre-adipocytes, there is a rapid and transient elevation in C/EBPb and C/EBPd [7,9] The appearance of these proteins is followed rapidly by the expression of C/EBPa, and by the nuclear hormone receptor peroxisome proliferator-activated receptor g (PPARg). These two factors remain elevated for the rest of the differentiation process and indeed for the life of the mature adipocyte. C/EBPa and PPARg are the most critical factors yet discovered for adipogenesis, as will be discussed below. For the moment, suffice it to say that virtually every single downstream target gene whose expression defines the adipocyte appears to be regulated by one or both of these proteins. All of the aforementioned factors, C/EBPa, C/EBPb, C/EBPd, and PPARg, can induce or accelerate differentiation in non-adipogenic NIH-3T3 cells [7].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15936931

RA609azQ naBxHk2qoqLRVDZI79XgO9S1rRHR3a77uXrY
has assertion: gtp(p(HGNC:HRAS)) -> p(HGNC:ADI1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.851+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> p(HGNC:ADI1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

5
value: Of the 80 protein spots showing significant changes in protein levels after oncogenic transformation by RAS, we successfully identified 32 of them from 34 protein spots by peptide mass fingerprinting.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RA1lr3ZjEbYYJOieJuuIo00ukOfglznt E ZYYTM1NfxM
has assertion: gtp(p(HGNC:HRAS)) -> p(HGNC:ECHS1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.861+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> p(HGNC:ECHS1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

5
value: Of the 80 protein spots showing significant changes in protein levels after oncogenic transformation by RAS, we successfully identified 32 of them from 34 protein spots by peptide mass fingerprinting.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RA38aVIM1VkdeifeI1-gojIwYZxm1TxjcGS0z3DmL9SUM
has assertion: gtp(p(HGNC:HRAS)) -> p(HGNC:GLO1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.862+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> p(HGNC:GLO1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

5
value: Of the 80 protein spots showing significant changes in protein levels after oncogenic transformation by RAS, we successfully identified 32 of them from 34 protein spots by peptide mass fingerprinting.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RAwvZ6fMoHIHJHtPJ1SKviZKUqJTOs6JHMkh4SbcI913A
has assertion: gtp(p(HGNC:HRAS)) -> p(HGNC:GAMT)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.863+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> p(HGNC:GAMT)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

5
value: Of the 80 protein spots showing significant changes in protein levels after oncogenic transformation by RAS, we successfully identified 32 of them from 34 protein spots by peptide mass fingerprinting.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RA6OiEZKB60 EesOGCbdkZz3Qa5HHSGIAxysO6fp89cPQ
has assertion: gtp(p(HGNC:HRAS)) -> path(SDIS:"anchorage-independent growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.877+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> path(SDIS:"anchorage-independent growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

4
value: While T29 cells, stably transfected with SV40 T/t antigens and hTERT, are fully immortalized, only the addition of oncogenic RAS leads to the malignant transformation of T29H cells as demonstrated by the capability of anchorage-independent growth and tumor formation in nude mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RA5VMIbPE3VJ1V5vulokxRjtsxp2bXjMa OXiZA9 Bgtg
has assertion: gtp(p(HGNC:HRAS)) -> path(SDIS:"tumor growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.878+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:HRAS)) -> path(SDIS:"tumor growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15940260

4
value: While T29 cells, stably transfected with SV40 T/t antigens and hTERT, are fully immortalized, only the addition of oncogenic RAS leads to the malignant transformation of T29H cells as demonstrated by the capability of anchorage-independent growth and tumor formation in nude mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15940260

RAxT4ziI SPrDNcOvW8a57xdH1fe sbaG8w7Lc2IeVuV4
has assertion: path(SDIS:"food intake") -| r(HGNC:PTPRA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.885+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(HGNC:PTPRA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 3 Genes up-regulated by diet
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RAzgkiWzwd N2xIBUAWPq5DaCoVe97h7YC02d7Go9Xbcw
has assertion: path(SDIS:"food intake") -| r(HGNC:RFC1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.888+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(HGNC:RFC1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 3 Genes up-regulated by diet
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RAz751uiWWRcivuSkq9VzOr4wKfphnMRYyxO1k0fd cQo
has assertion: path(SDIS:"food intake") -| r(HGNC:RARS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.889+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(HGNC:RARS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 3 Genes up-regulated by diet
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RAyTQsny7VnPo8vRUtyutqBTA8fzlK65w474CPtGMIJmI
has assertion: path(SDIS:"food intake") -| r(HGNC:RNASE4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(HGNC:RNASE4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 3 Genes up-regulated by diet
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RA8Y29y3c8ghhHx-cztV4oHD4FxjFu00 K7PF6oiv9Fzo
has assertion: path(SDIS:"food intake") -| r(HGNC:UGDH)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.893+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(HGNC:UGDH)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 3 Genes up-regulated by diet
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RAzQtKzhFk KegBMdMXrrHqdSvqXjyKeQRWPzVRgo7z-U
has assertion: path(SDIS:"food intake") -> r(HGNC:GLB1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.906+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(HGNC:GLB1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 4 Genes down-regulated by diet1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RAzRkjKEoRWMwcChMpTGTmqjVZqiEUe2T9aFesRCwhtiM
has assertion: path(SDIS:"food intake") -> r(HGNC:LYPLA1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.908+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(HGNC:LYPLA1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15941876

3
value: TABLE 4 Genes down-regulated by diet1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15941876

RA82ZflW8dKoaj9vg6GUDrFZEUIHru0G8jriVIVyASSr0
has assertion: p(HGNC:IL10) -> tscript(p(HGNC:STAT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.916+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL10) -> tscript(p(HGNC:STAT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15944287

5
value: By using specific inhibitors for PI3K (LY294002) and ERK MAPKs (PD98059), we demonstrate that LY294002 either alone or in conjunction with PD98059 inhibited IL-10-induced phosphorylation of STAT-1 and consequently CD14 expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15944287

RAzZRXrOBFBevy zCsxXBsKKUCLWt1xM4-eo7QYFKMJdM
has assertion: cat(p(MGI:Ctss)) -> (p(MGI:Ifng) -> bp(GO:"inflammatory response"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.924+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Ctss)) -> (p(MGI:Ifng) -> bp(GO:"inflammatory response"))
label: p(MGI:Ifng) -> bp(GO:"inflammatory response")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15944319

6
value: Selective cathepsin S inhibition and a null mutation of cathepsin S also decreased IFN-gamma-induced DNA injury, apoptosis, emphysema, inflammation, and protease accumulation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15944319

RAxyVdi-ozGT9DVgY5h2Nuxhn4b1QqHQJyv5ZWzsP 4C0
has assertion: p(MGI:Cd200) -> cat(p(MGI:Cd200r1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.926+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cd200) -> cat(p(MGI:Cd200r1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15946251

5
value: CD200 (OX2) is a membrane glycoprotein that interacts with a structurally related receptor (CD200R) involved in the regulation of macrophage function.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15946251

RA 3zlI3mDy5jJkqX YFYQZIWL3WqJ OmxOSl81q1pfHY
has assertion: kin(p(PFH:"PRKA Family")) => p(HGNC:GRK1,pmod(P,S,21))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.930+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) => p(HGNC:GRK1,pmod(P,S,21))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15946941

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15946941

RAzx8v4vWdAlIlS I9vkjftQbaHc9sZW5JZJNuWP4R9Ck
has assertion: kin(p(PFH:"PRKA Family")) => p(HGNC:GRK7,pmod(P,S,23))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.932+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) => p(HGNC:GRK7,pmod(P,S,23))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15946941

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15946941

RA7rZfxcJCAa0RNUS1il3dy7fP-JO42yBTD11 cTPWeI0
has assertion: tscript(p(HGNC:RB1)) -> bp(GO:"cell differentiation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.935+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:RB1)) -> bp(GO:"cell differentiation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15949438

4
value: It [pRB] also coactivates certain non-E2F transcription factors and promotes differentiation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15949438

RA4wSzSZhAtZZhJj6cXyw6dM8nOBP3FK7NYLcsSD2XlNI
has assertion: kin(p(HGNC:MAPK3)) => p(HGNC:RPS3,pmod(P,T,42))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.945+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) => p(HGNC:RPS3,pmod(P,T,42))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15950189

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15950189

RAx7-GLfTZGgB71KT2Fa4el4eEhfQqhiq ZxxEQc86tw4
has assertion: p(HGNC:EGF) -> bp(GO:"cell migration")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.948+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> bp(GO:"cell migration")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951439

3
value: down-regulation of SphK2 in these cells completely eliminated migration toward EGF
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951439

RAwcIZ6ZbLB S4yHdKdYWwSVaSassTnHRmDNo8kO4uu84
has assertion: p(HGNC:EGF) -> p(HGNC:EPHA2,pmod(P,Y,588))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.954+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> p(HGNC:EPHA2,pmod(P,Y,588))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

4
value: The fold increase of these EphA2 tyrosines are just below the cutoff used.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA5Vpl5v1e7cK6NUTalNa76YpjMVgxTJbApix2tmoVv2k
has assertion: p(HGNC:EGF) -> p(HGNC:EPHA2,pmod(P,Y,594))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.956+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> p(HGNC:EPHA2,pmod(P,Y,594))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

4
value: The fold increase of these EphA2 tyrosines are just below the cutoff used.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA2wxfa6Yd fCx0Ral4cNJj7L45O0OoNDgeZF7toYyq8A
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:CTNND1,pmod(P,Y,321))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.969+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:CTNND1,pmod(P,Y,321))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RAwjg85miFdxmHwJqyjXl IorV6oWGmQCM i4TKyvwQ U
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:CAV1,pmod(P,Y,14))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.974+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:CAV1,pmod(P,Y,14))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA5r0c-BQlvQe7gIBWpqLFF2cpXAl90KZwRG-ECz LPs0
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:EFNB2,pmod(P,Y,330))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.977+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:EFNB2,pmod(P,Y,330))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA2gB4wfETTptkIu89zt8Ig1D 4QikzPw6QVQpUwunXxg
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:ITSN2,pmod(P,Y,552))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.986+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:ITSN2,pmod(P,Y,552))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA-D3BU 8gkn-9J1-owbZnvgz-ftx1YBQltYTccuxm0Jo
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:NCK1,pmod(P,Y,105))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:35.992+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:NCK1,pmod(P,Y,105))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA2NqgNYaZL2u6fsNJBOywIctOMm M9wKwhV0oZML66U4
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:STAM2,pmod(P,Y,374))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.002+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:STAM2,pmod(P,Y,374))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA6ItOQzFL7c4KaZQ 4F6aXGfDCOO04CvZo7WaTdFhleo
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:TNK2,pmod(P,Y,857))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.008+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:TNK2,pmod(P,Y,857))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA5jv6MdB1vYr9LbtOSG0rFJ5buZbtjVFdovALSGLp iY
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:TNK2,pmod(P,Y,858))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.010+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:TNK2,pmod(P,Y,858))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RAzmXyVv7NOqceZbwyJNrWwfSkQLfT3VP4UIJx3ptFI7M
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:TNS3,pmod(P,S,536))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.012+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:TNS3,pmod(P,S,536))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA0DPfxmEfI SVXtMEPvtliZRXT6H sLuBTSHUHOUpDqo
has assertion: kin(p(HGNC:EGFR)) -> p(HGNC:TNS3,pmod(P,Y,540))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.013+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> p(HGNC:TNS3,pmod(P,Y,540))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15951569

5
value: This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15951569

RA4VMl-0tlYBeSam1wOXvCkfs2cBOtK5zBI6LlPwbKb08
has assertion: kin(p(HGNC:MAPK3)) => p(HGNC:GRB10,pmod(P,S,476))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.020+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) => p(HGNC:GRB10,pmod(P,S,476))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15952796

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15952796

RA4KKs-ARh9hGAidHevpH6saOomOIWgasRAAv-6quJLRE
has assertion: kin(p(PFR:"Prkc Family")) -> path(SDIS:"tumor growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.027+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Prkc Family")) -> path(SDIS:"tumor growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15953715

4
value: 4]. On the whole, these data are consistent with the known role of PKC isoenzymes in tumour cell proliferation, invasion and metastasis. Moreover, PKC has been implicated in the pathogenesis of asthma
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15953715

RAzB0J4PvqRBwLCAT1qWq7x9LUgAih2oqbIwUXbB3sfq8
has assertion: a(SCHEM:Sirolimus) -| p(HGNC:EIF4EBP1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.037+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Sirolimus) -| p(HGNC:EIF4EBP1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15956968

3
value: rapamycin inhibited phospho-RPS6 and 4E-BP1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15956968

RAxmecGoHz6h54TdbNr52ua499AsRnTUkcEfBdbSAlmN8
has assertion: a(SCHEM:Sirolimus) -| p(HGNC:RPS6,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.038+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Sirolimus) -| p(HGNC:RPS6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15956968

3
value: rapamycin inhibited phospho-RPS6 and 4E-BP1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15956968

RA9Ub7VtF-rjsH5J9 wrW17smqtL3O i5VJ0jyAXkg1aE
has assertion: p(HGNC:PTK2) -> p(HGNC:PXN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.047+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PTK2) -> p(HGNC:PXN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15963258

4
value: PRL stimulated (100 ng/ml for 15 min) the phosphorylation of paxillin by Fak in T47D cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15963258

RA3rI QRMZev7Ave1t0ng1wKKDO8sVdGjaumOCiJAkeBE
has assertion: a(SCHEM:Calcium) -| r(HGNC:UHRF1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.051+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Calcium) -| r(HGNC:UHRF1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964557

3
value: ICBP90 expression was strongly decreased after TCR triggering concomitantly to cyclin D3 and topoisomerase IIalpha expression decreases. Cell stimulation with PMA and/or calcium ionophore A23187 down-regulated ICBP90 expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964557

RA tl0sUZ lWgR-Kpcw9Wj4zEs6C6WtRj4WfnUSOrSRcU
has assertion: p(MGI:Gh) -> r(MGI:Igf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.053+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Gh) -> r(MGI:Igf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964559

4
value: Northern and Western blot analysis detected significantly higher levels of IGF-1 in cells overexpressing GH.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964559

RA1bJXmxw9UIWnAjLmj4Tjg1UHtxCacWmr3lhSYUce-6g
has assertion: tscript(p(HGNC:NR4A3)) -> bp(GO:"inflammatory response")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.058+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:NR4A3)) -> bp(GO:"inflammatory response")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964844

4
value: NR4A nuclear receptors as potential transcriptional mediators of inflammatory signals in activated macrophages
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964844

RAy93B3UuVoN-nSJ7jcqSPrX28e3jJvJRSXo25pF1ffo4
has assertion: tscript(complex(NCH:"Nfkb Complex")) -> r(HGNC:NR4A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.059+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCH:"Nfkb Complex")) -> r(HGNC:NR4A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964844

4
value: Several lines of evidence point to the NF-kappaB signaling pathway as a principal mediator of inducible NR4A expression in macrophages
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964844

RA1vgMXL-oQmW02MCHSay xlrLM g67Y0qSGi-GfJcyzA
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(HGNC:NR4A2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.065+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(HGNC:NR4A2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964844

3
value: Treatment of macrophages with lipopolysaccharide (LPS), cytokines, or oxidized lipids triggers the transcriptional induction of Nur77 (NR4A1), Nurr1 (NR4A2), and NOR1 (NR4A3) expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964844

RA-fooozHcRyABtWoPoZSXW-Qy8RtrY3CHpSwf2BP5dfs
has assertion: cat(p(HGNC:PRMT1)) -> tscript(p(HGNC:PPARGC1A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.070+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:PRMT1)) -> tscript(p(HGNC:PPARGC1A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15964996

6
value: PGC-1alpha coactivator activity is potentiated by arginine methylation by protein arginine methyltransferase 1 (PRMT1), another nuclear receptor coactivator.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15964996

RA6MDutjEQPnYOhGJ X4jUGOfBKSt2-eQ8huwR5kENW1U
has assertion: bp(GO:"response to osmotic stress") -> r(HGNC:AKR1B1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.077+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to osmotic stress") -> r(HGNC:AKR1B1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15965902

3
value: The cellular response to osmotic stress ensures that the concentration of water inside the cell is maintained within a range that is compatible with biologic function. Single cell organisms are particularly dependent on mechanisms that permit adaptation to osmotic stress because each individual cell is directly exposed to the external environment. Mammals, however, limit osmotic stress by establishing an internal aqueous environment in which intravascular water and electrolytes are subject to sensitive and dynamic, organism-based homeostatic regulation. Recent studies of NFAT5/TonEBP, an essential mammalian osmoregulatory transcription factor, demonstrate the unexpected yet critical significance of cell-based osmotic regulation in vivo. These results highlight the fundamental importance of maintaining intracellular water homeostasis in the face of varying cellular metabolic activity and distinct tissue microenvironments.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15965902

RA7cWQGunassM-jefq0ga zGV0CpJPrpwQJMbhs2R6Tx0
has assertion: p(HGNC:TP53) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.087+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TP53) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15967108

3
value: Biologically, SAK RNA interference (RNAi) silencing induced apoptosis, whereas SAK overexpression attenuated p53-induced apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15967108

RA9MJykcEF7L115qxtXPLai41SqKMX0sMKTAtNkNVV8oM
has assertion: p(HGNC:TGFA) => kin(p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.091+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFA) => kin(p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15967120

5
value: Both EGFR and GRPR are activated in NSCLC by their corresponding ligands, TGF-a and GRP, in an autocrine manner.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15967120

RA9n2s oLS2vpvVE2RUco6dQd C2FGaSPos3jWPXl6Zr0
has assertion: tscript(p(HGNC:BHLHE40)) -| r(HGNC:PER2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.108+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:BHLHE40)) -| r(HGNC:PER2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

5
value: From full text of Table 1 and following up on references in table 1: A list of potential BHLHB2- and BHLHB3-target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RA4ffgwz-7G2DsnkaFH4O lu6NysEK7r7eQ11DfcDt0kY
has assertion: tscript(p(HGNC:BHLHE40)) =| r(HGNC:MYC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.113+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:BHLHE40)) =| r(HGNC:MYC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

5
value: From full text of Table 1 and following up on references in table 1: A list of potential BHLHB2- and BHLHB3-target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RA-cDSj2vFnIAU q2qaNynYJT3S3oA8SlmSTeV NJkCY
has assertion: tscript(p(HGNC:BHLHE40)) =| r(HGNC:PCK2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.114+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:BHLHE40)) =| r(HGNC:PCK2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

5
value: From full text of Table 1 and following up on references in table 1: A list of potential BHLHB2- and BHLHB3-target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RA1r66n4BVG-zt5YUDyGlrnhsNHjopvqK--E8EfS-CKQE
has assertion: p(PFH:"PDGF Family") -> r(HGNC:BHLHE40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.169+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFH:"PDGF Family") -> r(HGNC:BHLHE40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

4
value: From full text table 4: Reagents regulating expression of the BHLHB2 and BHLHB3 genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RA5ch1br7FP-y1FVccqIo3lyiHrR7fV2utrk9Vc88QuSU
has assertion: a(CHEBI:glucocorticoid) -| r(HGNC:BHLHE40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.171+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:glucocorticoid) -| r(HGNC:BHLHE40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

3
value: From full text table 4: Reagents regulating expression of the BHLHB2 and BHLHB3 genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RA1IhJpQgimi0xnBMpGdpjEKDQb1pqPnRtACm87EtXEMM
has assertion: p(EGID:3630) -> r(HGNC:BHLHE40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.173+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:3630) -> r(HGNC:BHLHE40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15970569

4
value: From full text table 4: Reagents regulating expression of the BHLHB2 and BHLHB3 genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15970569

Selventa

RAxeC6 uDA8nsBvunVivszD3zoNYDr6kdD93215ft8e6U
has assertion: bp(GO:"cell differentiation") -> r(HGNC:ATP2A3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.179+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"cell differentiation") -> r(HGNC:ATP2A3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15972967

3
value: We report that SERCA3 expression increased along the crypts as cells differentiated in normal colonic mucosa
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15972967

Selventa

RA7a33Q-ht4HbEhimImsWrbmEV89 4XmPb5lbDsLGQOAo
has assertion: a(CHEBI:progesterone) -> r(HGNC:GPSM2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.190+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(HGNC:GPSM2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15976005

3
value: Supplemental Table 1 - genes regulated by progesterone at 48h up genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15976005

Selventa

RAxbDTavHzsk85UmvxUF33UZmjRJvmaj7Jd5oU6030UXo
has assertion: a(CHEBI:progesterone) -> r(HGNC:HSD11B2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(HGNC:HSD11B2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15976005

3
value: Supplemental Table 1 - genes regulated by progesterone at 48h up genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15976005

Selventa

RA 8h13CBxLqC-eUXlhzZHPR6YanYWtceoCJUFZ0nqngY
has assertion: a(CHEBI:progesterone) -> r(HGNC:MYC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.194+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(HGNC:MYC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15976005

3
value: Supplemental Table 1 - genes regulated by progesterone at 48h up genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15976005

Selventa

RAzJeFZozWeyTKRTlN4aT0iUwUR89oiqS6NAd4VsY0raQ
has assertion: a(CHEBI:progesterone) -> r(HGNC:PPP2CB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.195+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(HGNC:PPP2CB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15976005

3
value: Supplemental Table 1 - genes regulated by progesterone at 48h up genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15976005

Selventa

RA2r2WnQSQ7 pGL4SVsQ TDyo1Q7DxYR--dQWYWnW6Yn0
has assertion: a(SCHEM:"cyclic AMP") -> r(HGNC:HIF1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.210+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -> r(HGNC:HIF1A)
label: tscript(p(HGNC:MITF)) -> (a(SCHEM:"cyclic AMP") -> r(HGNC:HIF1A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15983061

6
value: melanocyte-specific transcription factor, microphthalmia-associated transcription factor (MITF), binds to the Hif1a promoter and strongly stimulates its transcriptional activity. Further, MITF \"silencing\" abrogates the cAMP effect on Hif1a expression, and overexpression of MITF in human melanoma cells is sufficient to stimulate HIF1A mRNA
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15983061

Selventa

RAwFbcI8rYUZdBcWHknS3MYi3J6JlWCB0neV90o8QAhJA
has assertion: p(HGNC:AKT2,pmod(P,S,474)) => kin(p(HGNC:AKT2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.222+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AKT2,pmod(P,S,474)) => kin(p(HGNC:AKT2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987444

5
value: After PIP3 binding, Akt1 is activated by phosphorylation on two critical residues, namely threonine %308 (T308) and serine 473 (S473); similar activation residues (S472 and S474, %respectively) are highly conserved in Akt2 and Akt3 Phosphoinositol-3-phosphate (PIP3) is a product of phosphoinositol 3-kinase enzymatic activity and has been shown to be a prerequisite lipid modulator of Akt activity Akt activity can be regulated by the PTEN tumour suppressor gene, which negatively regulates PIP3 levels PIP3 has been described as a downstream component of a wide range of receptors, including the c-Met receptor [5], the epidermal growth factor receptor family [6], fibroblast growth factor receptor [7], insulin growth factor receptor [8] and platelet-derived growth factor receptor
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987444

Selventa

RAwXW68Pa3qwOViNJaGL3azivH5Lo9GzyWHXLIaBxGYNg
has assertion: p(HGNC:AKT2,pmod(P,T,309)) => kin(p(HGNC:AKT2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.224+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AKT2,pmod(P,T,309)) => kin(p(HGNC:AKT2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987444

5
value: After PIP3 binding, Akt1 is activated by phosphorylation on two critical residues, namely threonine %308 (T308) and serine 473 (S473); similar activation residues (S472 and S474, %respectively) are highly conserved in Akt2 and Akt3 Phosphoinositol-3-phosphate (PIP3) is a product of phosphoinositol 3-kinase enzymatic activity and has been shown to be a prerequisite lipid modulator of Akt activity Akt activity can be regulated by the PTEN tumour suppressor gene, which negatively regulates PIP3 levels PIP3 has been described as a downstream component of a wide range of receptors, including the c-Met receptor [5], the epidermal growth factor receptor family [6], fibroblast growth factor receptor [7], insulin growth factor receptor [8] and platelet-derived growth factor receptor
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987444

Selventa

RA8ehn1nZNlzOOaH8jO42BhO8tG9S4u8kWyy8mXpTp1PU
has assertion: phos(p(HGNC:PTEN)) =| a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.232+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTEN)) =| a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987444

4
value: Akt activity can be regulated by the PTEN tumour suppressor gene, which negatively regulates PIP3 levels
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987444

Selventa

RA6IyP55HeuMQTO6ADqdAfU63lOuS4IJ14eEEULZKV3Kk
has assertion: kin(p(HGNC:FGFR1)) -> complex(a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate"),p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.238+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FGFR1)) -> complex(a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate"),p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987444

6
value: PIP3 has been described as a downstream component of a wide range of receptors, including the c-Met receptor [5], the epidermal growth factor receptor family [6], fibroblast growth factor receptor [7], insulin growth factor receptor [8] and platelet-derived growth factor receptor
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987444

Selventa

RA5kcH6aXDt4wrGCxbOW46mIY2VQv1NXpvyPp OvE3PCo
has assertion: kin(p(HGNC:FGFR1)) -> kin(p(HGNC:AKT3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.241+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FGFR1)) -> kin(p(HGNC:AKT3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987444

6
value: PIP3 has been described as a downstream component of a wide range of receptors, including the c-Met receptor [5], the epidermal growth factor receptor family [6], fibroblast growth factor receptor [7], insulin growth factor receptor [8] and platelet-derived growth factor receptor
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987444

Selventa

RAwypxEIKx7L0l9ANNo0d6WQG23zfHi0J95iyydXWgFy4
has assertion: tscript(p(HGNC:ELF5)) => r(HGNC:KRT18)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.243+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ELF5)) => r(HGNC:KRT18)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15987600

5
value: title := \"Epithelium-specific ets transcription factor 2 upregulates cytokeratin 18 expression in pulmonary epithelial cells through an interaction with cytokeratin 18 intron 1.\" Multiple interactions between the ETS domain and putative DNA binding sites within K18 intron 1 were observed,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15987600

Selventa

RA9-qnN2M549BMVuFAANxcMjh58fcg7QZ9bqeHzY7 Mg0
has assertion: tscript(p(MGI:Nfe2l1)) -| r(MGI:Cops5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.248+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Nfe2l1)) -| r(MGI:Cops5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988009

5
value: Fra-1 and JAB1 (COPS5) levels are markedly increased in Nrf1 and Nrf2 null cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988009

Selventa

RA3DjGlSuuAUcEhZxrRJJWsLfWlMOpYjenBp0LBGN0ivk
has assertion: tscript(p(MGI:Nfe2l1)) -> r(MGI:Gclc)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.251+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Nfe2l1)) -> r(MGI:Gclc)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988009

5
value: Glutamate-cysteine ligase catalytic subunit (GCLC) is regulated transcriptionally by Nrf1 and Nrf2.tert-Butylhydroquinone (TBH) induces human GCLC via Nrf2-mediated trans activation of the antioxidant-responsive element (ARE). Interestingly, TBH also induces rat GCLC, but the rat GCLC promoter lacks ARE. This study examined the role of Nrf1 and Nrf2 in the transcriptional regulation of rat GCLC. The baseline and TBH-mediated increase in GCLC mRNA levels and rat GCLC promoter activity were lower in Nrf1 and Nrf2 null (F1 and F2) fibroblasts than in wild-type cells.Overexpression of Nrf1 and Nrf2 in respective cells restored the rat GCLC promoter activity and response to TBH but not if the AP-1 and NF-kappaB binding sites were mutated.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988009

Selventa

RAzo6yIUljxUVENgLv W5l-hZlj8NTcQVM5TZuTG6mGAQ
has assertion: tscript(complex(NCM:"Nfkb Complex")) => r(MGI:Gclc)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.253+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) => r(MGI:Gclc)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988009

4
value: Nrf2 overexpression alone also induced the rat GCLC promoter activity and, in conjunction with TBH treatment, resulted in a synergistic induction of the rat GCLC promoter activity. However, this induction is blocked significantly if the AP-1 site or the NF-kappaB site is mutated and completely prevented if both sites are mutated.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988009

Selventa

RAyb1wadi7rF18WAn kxEX8M0ZHmTLjcyzkDnG3dFfkQk
has assertion: tscript(p(MGI:Nfe2l2)) -> tscript(complex(NCM:"AP-1 Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.255+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Nfe2l2)) -> tscript(complex(NCM:"AP-1 Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988009

5
value: Nrf2 overexpression alone also induced the rat GCLC promoter activity and, in conjunction with TBH treatment, resulted in a synergistic induction of the rat GCLC promoter activity. However, this induction is blocked significantly if the AP-1 site or the NF-kappaB site is mutated and completely prevented if both sites are mutated.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988009

Selventa

RA2BSdfUtGhqjuTe28qJwKh6lkfwgbxsgmDo89caYJKog
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:BBC3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.278+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:BBC3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAw9AsBT3HiiDNr7uaqmlhJ94w2YKzdm9XCb-B8-AoLp0
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:BIK)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.280+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:BIK)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA1w1qnpmODgI8iE1l ivyhV3HfEaAflic6Kymjl FbdE
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:COL17A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.290+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:COL17A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA3fvS0KCjinJJmG327ArnalEJyLfs91bTvsHHR3oAEXM
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:CRIP2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.292+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:CRIP2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAxTk0XFZpZchmwc441CNzooYclsYRjSoIQU7ZKBailnw
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:CX3CL1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.295+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:CX3CL1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA8O6IuTppWKFqnhGYKtcmH0EEWvWd8pC0GqeXIjc8LV8
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:CDC42EP4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.296+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:CDC42EP4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA9eh4uKqJ9zQsIDu1UAYyJBfShvQWW4ZfreAichPfrqU
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:CEL)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.297+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:CEL)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAw1wSRkD8zw6MZ4jwkro-VpXwD4Fi6DCvQxVTTo6nobg
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:EPHB3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.309+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:EPHB3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAxl0Gt5GAegvzs S5WKclYlMEwrGwek3tdk8Hkn5G208
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:FDXR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.312+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:FDXR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAwFHT1bTkTPYKyk9DwdeP8PTxQO5OIiY7BM4rv Nzz7A
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:FEZ1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.314+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:FEZ1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAwXg4-TXArffSP3aal mW8NfRx537wOi26D8qMu10vFA
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:GAS6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.323+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:GAS6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA3tGPxJy1dyBO4xcYLeKoZTbQxiN1isGnORfMldL 1eQ
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:GGT1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.327+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:GGT1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA6rBthGpkIzV5lEOLcPxr90IF2lChii-uDLL8helCLzo
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:GRIN2C)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.331+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:GRIN2C)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAwdl7D4OLjWPAEUiU1CtW20F8dSrL668rmDevdk-tkDs
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:GAMT)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.333+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:GAMT)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA0mTXJNOejbKBgDxqLAJ6D ekxaZLHpZjgSoJD1A4GUM
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:HSPG2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.335+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:HSPG2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA5sx 2 D-ZOsxiju1XyvmU6QaZOfkVfgqpvalcjoY14o
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:ITPKC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.346+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:ITPKC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA8F1Fj23fE3yXoRl7nbmPRdn4wS9lwvXHSHVRcaQznU8
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:IRF1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.347+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:IRF1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAxOkcBItJ2hPBRXXLG77eZrtLIc5ixPGw7UY9YGPuD2o
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:JAG2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.350+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:JAG2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA77Qdt2Olfs8yChdYRgbtx KhtUNaQBNsTADmkvWYYJM
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:KCNK3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.353+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:KCNK3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA UOfozeM8arv4nPK mJnz6sE6RmMUkPxqGgkzk4 yTc
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:LAMP3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.354+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:LAMP3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAynx-d5gi-4vdfvcLIJbLbV7Cl59YJ-knWl5abepR1zk
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:MAST4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.357+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:MAST4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAy0Dn9L1l8eiAWkASmiSzLk9UmoThtd93uUEjTeUePGU
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:MERTK)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.360+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:MERTK)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA vZtgKAmdYXTD4h5 5ZdV77W3Nb4jF4AqXJs5zLvfPA
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:NT5E)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.371+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:NT5E)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA4QJiS5BljkcMldBtnet7tJZf4ZNrmjr2pf9XYThEyGw
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:NGFR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.372+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:NGFR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA L5b6VOCUekXijdxAvVod8vChMhMMg8ze4zUojVx2A8
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:PDLIM7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.373+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:PDLIM7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA8s BFdxMJblAXQWEGvraq6mcgzuGzOqIGBJbsOL2xjM
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:PRICKLE3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.380+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:PRICKLE3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA6ngySQrjsFuERPBdvQUshNR6XclqPIyFgYkqTeXXLsI
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:PTPN3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.385+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:PTPN3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA9bZOrsO3 fq-oIr38JgVyxBSYEHZ49JZ-gi5MFLssqc
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:PGF)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.387+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:PGF)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAxn-jhc-l0ZSE-Uo-4nbZMCS3jrB7Tpno2s22Cb12gc4
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:RAP1GAP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.392+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:RAP1GAP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA3v6ka5ZIyPWEBUoM2F7HSo-sxlsJ3XytEQCO0C-nOIk
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:SFN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.402+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:SFN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA3jqv8kqWRq-IyYmjiOgP-uBgcsD2jXSuWN60vMixz9g
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:SDC1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.412+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:SDC1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RAziF2msf1EZanZ OUELZWXwpqX6aQNQbCTrplKAaFcz8
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:TOB2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.416+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:TOB2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA3PJCKtvJ-06OMXDZEioy7tg44u6V 11c15UJBTPUScQ
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:TSPAN4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.423+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:TSPAN4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15988020

5
value: By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. # TABLE 1. List of genes induced over fourfold by TAp63y in 293 inducible cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15988020

Selventa

RA7f7jqHTa8C5wQT3jjKsW1V-hNItmv-jzCy 3RwtAymY
has assertion: p(HGNC:IFNG) -> p(HGNC:C3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.432+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IFNG) -> p(HGNC:C3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15989786

4
value: TNF-alpha, IL-1beta, IL-6 and IFN-gamma could induce the secretion of C3 and Bf of A549 cells. RA alone had no effect on secretion of C3 and Bf of A549 cells but could notably enhance the secretion of C3 and Bf of A549 cells induced by the cytokines
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15989786

Selventa

RA0eXP-Mu6pgxNZWpTkLC2KlVRkzn3h6uNtt4Ntm lmSQ
has assertion: a(SCHEM:Tretinoin) -> (p(HGNC:TNF) -> p(HGNC:CFB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.442+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> (p(HGNC:TNF) -> p(HGNC:CFB))
label: p(HGNC:TNF) -> p(HGNC:CFB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15989786

5
value: TNF-alpha, IL-1beta, IL-6 and IFN-gamma could induce the secretion of C3 and Bf of A549 cells. RA alone had no effect on secretion of C3 and Bf of A549 cells but could notably enhance the secretion of C3 and Bf of A549 cells induced by the cytokines
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15989786

Selventa

RA5CAy1uuBTbj5iefRlHstV5f2682BlSrQ03IUDrXwqvc
has assertion: a(CHEBI:"zinc protoporphyrin") -| cat(p(MGI:Hmox1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.447+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"zinc protoporphyrin") -| cat(p(MGI:Hmox1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15993853

4
value: NO-mediated increase in MnSOD activity was partly abolished by HO-1 inhibitor Zn(II) protoporphyrin IX (ZnPP)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15993853

Selventa

RA9xYPW-C5i3gZPoWhysSU9TNB 5 CYgIuLEmPZQPBaRg
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> sec(p(PFH:"HSPA Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.450+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> sec(p(PFH:"HSPA Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15993884

4
value: After 24 h there was a significant increase in HSP70 in the culture media of oxLDL treated macrophages compared to untreated controls (P < 0.05, Fig. 2A and B).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15993884

Selventa

RAzoPKApTgQmME1HCcHZTHl3m8rUygGUBWXj9GGhpUWio
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> sec(p(PFH:"HSPA Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.454+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> sec(p(PFH:"HSPA Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15993884

4
value: OxLDLsup increased intracellular IL-12 production in naïve macrophages (P < 0.05; Fig. 5), and pre-treatment of the oxLDLsup with neutralizing antibodies against HSP70 inhibited this increase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15993884

Selventa

RAz44O3KBBkxDlEAF7EQ0m1eT2ElgxBUKRND0eMMnj8PE
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(HGNC:HMOX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.456+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(HGNC:HMOX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15993884

3
value: The results from the DNA microarray scan show that 5 of the 17 up regulated genes after 6 h of oxLDL treatment belonged to the heat shock protein (HSP) family (Fig. 1A). Three of these genes belonged to the HSP70 family (HSP70-1A, -1B and HSP70 6). The two remaining HSP genes were DNAJB1 (member of the HSP40 family) and heme oxygenase 1 (HMOX1, also referred to as HSP32).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15993884

Selventa

RAxo9z6CshOdXaHg2a6Rjp6860itF4xtyEbekKCggmxhU
has assertion: a(CHEBI:lipopolysaccharide) -> r(HGNC:IL1R1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.458+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(HGNC:IL1R1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15994259

3
value: Figure 1 Gene expression in peripheral blood neutrophils stimulated by several mediators in vitro. (RT-PCR) Peripheral blood neutrophils were incubated with several physiological stimuli for 3 hours in vitro at 37?C (TNFa, 100 U/ml; GM-CSF, 0.1 nM; IL-8, 10 nM; fMLP, 1 mM; LPS, 10 ng/ml). Expression of indicated genes was measured by real time RT-PCR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15994259

Selventa

RA-Ey0VKpjHvxwOru5qRnnZo07tDwlSIQqrMXtrZlT04w
has assertion: a(CHEBI:lipopolysaccharide) -> r(HGNC:IL1R2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.459+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(HGNC:IL1R2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15994259

3
value: Figure 1 Gene expression in peripheral blood neutrophils stimulated by several mediators in vitro. (RT-PCR) Peripheral blood neutrophils were incubated with several physiological stimuli for 3 hours in vitro at 37?C (TNFa, 100 U/ml; GM-CSF, 0.1 nM; IL-8, 10 nM; fMLP, 1 mM; LPS, 10 ng/ml). Expression of indicated genes was measured by real time RT-PCR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15994259

Selventa

RAzHSVDsZjmfN8BHGJAZJz-oGGmv2DJaJsCKyFc1yAllg
has assertion: p(EGID:209446) -> r(MGI:Wt1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.463+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:209446) -> r(MGI:Wt1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15994295

4
value: TFE3 and TFEB regulate endogenous WT1, Snail, and Smad7 expression in 3T3 cells. A, RT-PCR analyses indicate that overexpressed TFE3 and TFEB induce WT1 expression and decrease Snail expression in 3T3 cells; inhibition of endogenous TFE3 and TFEB represses Smad7 expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15994295

Selventa

RA2nnlv7kz5H6B5rEdGxKbE-t2Vg9sckVzas8W7IFxuCE
has assertion: cat(p(HGNC:LPL)) -> tscript(p(HGNC:STAT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.474+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:LPL)) -> tscript(p(HGNC:STAT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15994321

6
value: (Stat1). The anti-inflammatory response of LPL in suppressing TNF-alpha-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-alpha degradation and phosphorylation of the p65 subunit.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15994321

Selventa

RA xZueW5WoVS-P9WEqKnVVHbA-uDcxyNjiCPIiEH8sV0
has assertion: kin(p(HGNC:JAK2)) -> tscript(p(HGNC:STAT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.475+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:JAK2)) -> tscript(p(HGNC:STAT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15994321

6
value: (Stat1). The anti-inflammatory response of LPL in suppressing TNF-alpha-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-alpha degradation and phosphorylation of the p65 subunit.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15994321

Selventa

RA6 nYKZVwWpFryh7v2Ks65VYGCbovthGHLWPob8HVDUI
has assertion: complex(p(MGI:Mib1),p(MGI:Dll1)) -| p(MGI:Dll1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.497+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Mib1),p(MGI:Dll1)) -| p(MGI:Dll1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16000382

6
value: Mind bomb 1 (Mib1) has been identified as a ubiquitin ligase that promotes the endocytosis of Delta. In accordance with the pan-Notch defects in Mib1-/- embryos, Mib1 interacts with and regulates all of the Notch ligands, jagged 1 and jagged 2, as well as Dll1, Dll3 and Dll4.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16000382

Selventa

RA1dmT9qBR7Xkp9iIZkQIoV6WR5i0RsY8LSOXGosymvs4
has assertion: a(CHEBI:"reactive oxygen species") -> a(SCHEM:"8-Oxo-7,8-dihydrodeoxyguanine")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.501+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"reactive oxygen species") -> a(SCHEM:"8-Oxo-7,8-dihydrodeoxyguanine")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16002790

2
value: 8-Oxo-7,8-dihydroguanine (8-oxoGua) is produced in cells by reactive oxygen species
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16002790

Selventa

RA-t2HdC-eK7PsvgH7kUZ-iTwUxP19v8-DrsInDRYbRG4
has assertion: p(HGNC:KRAS,sub(Q,61,H)) => gtp(p(HGNC:KRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.502+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

1
has substitution: Q,61,H
variant of: http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=6407
type: http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00000

p(HGNC:KRAS,sub(Q,61,H)) => gtp(p(HGNC:KRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16003751

5
value: From mutations file
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16003751

Selventa

RAw5t7QcI5IDc9ILxjNx3FC3nLAjTwcUY2oli9WvNFjVE
has assertion: a(CHEBI:lipopolysaccharide) -> p(HGNC:TLR2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.509+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> p(HGNC:TLR2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16004610

3
value: cells were exposed to LPS (1 ?g/ml) which led to an increased expression of TLR2 on AM from nonsmokers (18.35 ± 4.24 vs. 13.98 ± 2.54 rMFI [A] p < 0.04; 21.1 ± 6.23 vs. 12.07 ± 3.5 [B] p < 0.04). In contrast, cells of smokers and COPD patients did not respond to LPS stimulation with increased TLR2 expression
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16004610

Selventa

RA1gwzQCc2 rvjjRg5wDCJGWveeb02xYBKH37okgpd2wc
has assertion: path(SDIS:"Type II diabetes") positiveCorrelation r(MGI:Sod1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.513+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"Type II diabetes") positiveCorrelation r(MGI:Sod1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16005359

3
value: GPx-1 and SOD-1 showed elevated mRNA expression in the KKAy mice in the kidney and heart,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16005359

Selventa

RA0BG sE qvAA1XVluPbpVNvQSZURRHaz4nSQHByUUit0
has assertion: bp(MESHPP:Obesity) positiveCorrelation p(MGI:Nampt)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.518+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation p(MGI:Nampt)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16005682

3
value: The significance of endogenous visfatin controlling whole-body insulin sensitivity is reinforced by the phenotype of lean, heterozygous visfatin-knockout mice, which revealed mild but reproducible hyperglycaemia. Subsequent analysis of this insulin-mimetic effect revealed two surprising findings: that the effects of visfatin are mediated by the insulin receptor itself, with remarkably similar affinities to those of insulin but through a distinct binding site, and that this insulin-sensitizing effect of visfatin might be additive to the effect of insulin, suggesting that visfatin activates insulin-receptor-activated pathways through a novel mechanism. What is the physiological relevance of visfatin for the metabolic syndrome? The discovery of this curious new adipokine has great potential to significantly enhance our understanding of the metabolic syndrome. However, as with most new discoveries, these findings need to be reproduced. Indeed, there is already an indication that the correlation between visfatin gene expression and the metabolic syndromemight not be universal to all models [8]. Novel findings also raise several newquestions that need to be addressed before their true significance can be appreciated. It will be necessary to determine the contribution of visfatin originating from visceral adipose tissue to the control of global insulin sensitivity. Although the affinity of visfatin for the insulin receptor appears to be similar to insulin, its concentration in plasma is much lower (3-10% of the insulin concentration) under physiological conditions. It is also not regulated by fasting and feeding. This raises doubts about the physiological importance of the systemic insulinsensitizing effects of visfatin. However, the dramatic elevation of visfatin levels in the visceral adipose tissue of obese mice suggests that it has a significant role in the pathophysiology of obesity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16005682

Selventa

RA8aof-u1L6TvQSPLhxBts0DSd0yLscJUWgh0AP15c63I
has assertion: p(HGNC:NAMPT) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.520+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NAMPT) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16005682

3
value: When delivered directly to diabetic mice, visfatin also improved insulin sensitivity in vivo, decreasing glucose and insulin levels [2].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16005682

Selventa

RA2ocQW0nk7opGkn4fuM-JugiEQnjogq1KZwc9lc2tNbw
has assertion: p(HGNC:MYD88) -> tscript(p(HGNC:IRF5))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.523+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MYD88) -> tscript(p(HGNC:IRF5))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006187

5
value: IRF5 associates with both Myd88 and TRAF-6 and ligands for TLR4 and TLR9 promote nuclear translocation of IRF5 in a Myd88-dependent manner [61] (Figure 3). However, many of the downstream mediators of the IRF5 pathway await identification. Although IRF-5 is phosphorylated by TBK1 and IKK-i, this phosphorylation does not lead to IRF-5 nuclear translocation or activation [62]. The Myd88 activation of IRF-5...
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006187

Selventa

RA94iAz28Dt0bomwkggnqNGVs2-lVMhDDhRpQlcfjM3mQ
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(MGI:Stmn1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.527+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> r(MGI:Stmn1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I Differentially expressed proteins in oxLDL-treated J774 or J774-CE macrophages
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAxk8b6poeRDrsgCQNwFyQKYV6 38fI1Bfd4HNVoL0hlo
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:12332)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.528+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:12332)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA0FosqwVxWIGWpkY12e55rxOwv6XK5Xyn8AQUHeuZS-4
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:11461)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.535+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:11461)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA9azQndboCgCqU3D1AnW QhQ3RCQveFIx6g1UjGqnSls
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:17886)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.551+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:17886)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA cZbKrg8ULuXfTnF8Kbvb3xUOoPD3uRjVZaRTDwEt-M
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18655)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.555+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18655)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA p5j4slvSjKnxMAA-gCv5axDnQI uXoLTxVt7BtsR5Y
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18746)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.557+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18746)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA0PktahE1pHWoTxVkTTL L-BWZhtIu5iURyw5UtJXh9s
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18746)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.558+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:18746)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA3QMcMInemZcU-Acvi77gdV1m7IC1Er-QsJ W-0h2un0
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:20655)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.559+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:20655)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA3uH3pj1xosLFphPZT6PfrevNxDoLi jBuBiN-4ix3kY
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:233016)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.563+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:233016)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE I - Differentially expressed proteins in oxLDL-treated J774. All identified proteins gave Mascot total scores greater than 200, which was calculated from the expression 10 log(p) where p is the probability that the match is a random event (p 1020). Individual peptide scores of 40 or greater represented extensive homology, and at least two of these CID spectra from each analysis were visually inspected to verify the peptide sequence. Typical sequence coverage was at least 20%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA7RSHwV1hS 7CVCXc08qdzMXT6nV0v91n6Cwk-psf-k
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:107146)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.564+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:107146)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE II - Up-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAyOAffaWsReO0nvXmowKNsQjklP89lS9pXKmMGwasoV0
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:20706)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.578+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:20706)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE II - Up-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA9CZcZcRGXWQcUpNlZgWaVDAvtoko H76SvCSnzmR bQ
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:52822)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.582+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:52822)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE II - Up-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA3wPbSbEkbo5L9eNTvuGd4C9XrIwVU9hmkzspKPzA5NI
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:59010)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.583+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:59010)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE II - Up-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA GLQ3x5RrLGAeb65A-JspqImwjJVtFHC0REOeucwqgg
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:108052)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.586+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:108052)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA3r0V7Lyn013vMTtxwJHqmMPTcsLrEw2iY4Ln4VVv4xA
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:22040)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.639+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:22040)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAwJWR9t1w-I72PRCP8W0ONFSvuYDRFqnqI9fuStvhq00
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:276950)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.647+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:276950)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA350UQdd3qeJA74yO0fWGiPIbbX16qmbNlG3T7Xhtqsg
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:327978)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.648+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:327978)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA8vJJg94HkDozuXWTOwZorXAy6hqg6EsF12ZFhSykUew
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:55932)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.652+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:55932)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAw75hICxWQBiQc3lTO2aeIYS6usn38c1agRPktLURsoo
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:65963)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.654+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:65963)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAzxCULIVpj5gQh8s 96TsREy1s0aYd-RnG8xyOS4B7GI
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:98660)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.659+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:98660)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE III - Down-regulated mRNA in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA9TL7L2tB0QU090RLSzJx59mf4qZ6onkzAODWnm8D5dg
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:211666)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.667+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:211666)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE IV - Differential regulation of antioxidant response genes in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA0tsvTCclXfuRV8xehgsdIL6sfA4simnJgDcCxM7JUcc
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:50493)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.668+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:50493)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE IV - Differential regulation of antioxidant response genes in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA8usZoVNvSVwNtl1A3dQwTyqvWUTWudL fv5cNMvf9O8
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:77974)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.670+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:77974)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE IV - Differential regulation of antioxidant response genes in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA3bagqz6YD0O1qglWtUNQnjxZKmq6uhEEtQwppG8b6HA
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:110454)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.671+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:110454)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAzyT9HUwwHcNs2nHaeQu3leuTgi60bW7txw-8GfPtbms
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:16019)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.679+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:16019)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA495O xMsyEztMacFSvUcmWy8IfiykXSKCuIIR JQVME
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:170744)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.685+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:170744)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA5G-aAQA8e1 8lLGaRALJXdBFEvRyzx52tpj-HMxc0MI
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:21810)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.688+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:21810)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA8 zwo-glfu8GAGZH4lfKNMi9Zc2wTxkqAJY H qWLJ0
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:23962)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.690+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:23962)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RA5NADs6VPl4lnxziVaJPLqaO1zfCV0PU1YWZ7rte8Z18
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:67775)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.695+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -| p(EGID:67775)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAyvulkqr3CSQaacTrQl4k74Xdgij1GPyMA6ZDYHFixLs
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:21939)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.702+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> p(EGID:21939)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006650

3
value: TABLE V - Differential regulation of immune response mRNA transcripts in oxLDL-treated J774 macrophages. The statistical significance of the differential expression for each transcript was determined by the Wilcoxon signed rank test. Each probe set in the differentially expressed sample was compared with its counterpart, and a p value was calculated to determine the degree of change. A value of p less than 0.002 denoted an increase in transcript, and a value of p greater than 0.998 denoted a decrease in transcript. All of the differentially expressed transcripts reported here were determined to be increased or decreased in the oxLDL-treated sample of at least one sample pair (J774 untreated/oxLDL-treated or J774-CE untreated/ oxLDL-treated) according to this statistical test.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006650

Selventa

RAw27s-WFD7kSttM4bTqM0DjTIytOQBzGbymzNfS 3d-g
has assertion: p(HGNC:CDKN1B) -| bp(GO:"cell cycle")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.705+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CDKN1B) -| bp(GO:"cell cycle")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006743

3
value: SIRT1 binds acetylated FOXO4 and restores its activity. Thus SIRT1 activates FOXO1 and FOXO4, which promote cell-cycle arrest by inducing p27kip
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006743

Selventa

RA5hZgeawfrG0FqcrV7vBVIpztpwn8ep-NTupdKrF69YU
has assertion: p(HGNC:NCOR2) =| tscript(p(HGNC:PPARG))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.707+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NCOR2) =| tscript(p(HGNC:PPARG))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16006743

5
value: SIRT1 represses PPAR-gamma, a key regulator of adipogenesis, by docking with its cofactors NCoR (nuclear receptor co-repressor) and SMRT (silencing mediator of retinoid and thyroid hormone receptors)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16006743

Selventa

RA xOXr1UsCckWIT7vvzi4aH7 2DmVcnNVC4CukW2ol4Y
has assertion: kin(p(MGI:Erbb4)) -> p(MGI:Errfi1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.720+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Erbb4)) -> p(MGI:Errfi1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007071

5
value: Although it has been clearly established that negative feedback loops have a fundamental role in the regulation of epidermal growth factor receptor (EGFR) signalling in flies, their role in the regulation of mammalian EGFR has been inferred only recently from in vitro studies. Here, we report on the forced expression of RALT/MIG-6, a negative feedback regulator of ErbB receptors, in mouse skin. Conversely, knockdown of RALT by RNA interference enhanced ErbB mitogenic signalling. Thus, RALT behaves as a suppressor of EGFR signalling in mouse skin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007071

Selventa

RAxJZEjMz2Ja8S1LR2oZ2DQUI08EK0Kcy7ciH8Nv9vr08
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:"adipose glucose import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.728+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:"adipose glucose import")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007182

3
value: Finally, activation of Akt induces an increase in the concentration of cellular fatty acids as well as phosphoglycerides, the components of cellular membranes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007182

Selventa

RA5-K3EBbjO9VEGw0iCvTNkxypzsdSquN9zSMN2OWiOMk
has assertion: kin(p(HGNC:AKT1)) -> tscript(p(HGNC:SREBF1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.733+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) -> tscript(p(HGNC:SREBF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007182

6
value: We also show that Akt leads to the accumulation of nuclear SREBP-1 but not SREBP-2, and that activation of SREBP is required for Akt-induced activation of the FAS promoter.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007182

Selventa

RA6zSyyAL5m70UJ-4Y57OK2xwU0g7 rWEUQrawOXXdl24
has assertion: bp(GO:"response to UV") -> r(HGNC:ID3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.736+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV") -> r(HGNC:ID3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007217

3
value: Id2 protein is selectively upregulated by UVB... which revealed that UVB alters the expression of three of the four human inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix family of transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. These results were verified by RT-PCR and immunoblot analysis of control and UVB-irradiated primary and immortalized keratinocytes. Whereas Id1 was downregulated in both cell types, Id2 expression was upregulated in primary HFK, but not immortalized cells. In contrast, Id3 expression was significantly increased only in immortalized cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007217

Selventa

RA1EVMdhMgU4T60 0aVfGvSG NzTcXsJWPuorodN2a0vE
has assertion: bp(GO:"response to UV-B") -| r(HGNC:ID1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.737+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV-B") -| r(HGNC:ID1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007217

3
value: Id2 protein is selectively upregulated by UVB... which revealed that UVB alters the expression of three of the four human inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix family of transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. These results were verified by RT-PCR and immunoblot analysis of control and UVB-irradiated primary and immortalized keratinocytes. Whereas Id1 was downregulated in both cell types, Id2 expression was upregulated in primary HFK, but not immortalized cells. In contrast, Id3 expression was significantly increased only in immortalized cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007217

Selventa

RA5nVSUSRsf0BkvVBoK0XENhcly808AOUirlSkhoSr0Tc
has assertion: bp(GO:"response to UV-B") -> r(HGNC:ID2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.739+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV-B") -> r(HGNC:ID2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007217

3
value: Id2 protein is selectively upregulated by UVB... which revealed that UVB alters the expression of three of the four human inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix family of transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. These results were verified by RT-PCR and immunoblot analysis of control and UVB-irradiated primary and immortalized keratinocytes. Whereas Id1 was downregulated in both cell types, Id2 expression was upregulated in primary HFK, but not immortalized cells. In contrast, Id3 expression was significantly increased only in immortalized cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007217

Selventa

RA-yU9T92uwiB38MWnGcHNYjRytZ9O793hQlmm9JEwNdI
has assertion: bp(GO:"response to UV-B") -> r(HGNC:ID3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.740+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV-B") -> r(HGNC:ID3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007217

3
value: Id2 protein is selectively upregulated by UVB... which revealed that UVB alters the expression of three of the four human inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix family of transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. These results were verified by RT-PCR and immunoblot analysis of control and UVB-irradiated primary and immortalized keratinocytes. Whereas Id1 was downregulated in both cell types, Id2 expression was upregulated in primary HFK, but not immortalized cells. In contrast, Id3 expression was significantly increased only in immortalized cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007217

Selventa

RA6s7jzgggE43ABAe5bQDtpbAS-W5YBuNWEGs7A1YouCo
has assertion: p(MGI:Olr1) -> path(SDIS:"fatty acid import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.743+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Olr1) -> path(SDIS:"fatty acid import")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007265

3
value: Increased OLR1 expression, resulting either from TZD treatment or adenoviral gene delivery, significantly augments adipocyte cholesterol content and enhances fatty acid uptake
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007265

Selventa

RA0h-eFGs8ya019LOwP1pdfO-TnkYFZyxgXwHDsZ-TCBA
has assertion: a(CHEBI:rosiglitazone) -> path(SDIS:"fatty acid import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.744+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:rosiglitazone) -> path(SDIS:"fatty acid import")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007265

2
value: Increased OLR1 expression, resulting either from TZD treatment or adenoviral gene delivery, significantly augments adipocyte cholesterol content and enhances fatty acid uptake
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007265

Selventa

RA-NZuBQzq5te-U1M1JwdxMohgBTQiKQ6R4ozIY99Wi04
has assertion: a(CHEBI:rosiglitazone) -| tscript(p(MGI:Ncor2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.748+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:rosiglitazone) -| tscript(p(MGI:Ncor2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16007265

4
value: SMRT and NCo-R were recruited to the 3 distinct regions in the OLR1 promoter containing the PPREs. Rosiglitazone treatment released corepressor binding in all 3 regions
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16007265

Selventa

RA6LCqjfwucVVE7XowaHMrkMNaPM4T4wBwQ8h oNqBBeM
has assertion: bp(GO:"cell differentiation") -| r(MGI:Brd3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.751+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"cell differentiation") -| r(MGI:Brd3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16008511

3
value: we identified three conserved but uncharacterized genes encoding bromodomain containing 3 (BRD3), protein lysine methyltransferase (PLM), and kelch domain containing 2 (KLHDC2), which were downregulated during endothelial differentiation. An RNA blot study showed that these genes were markedly expressed in undifferentiated ES cells, whereas the expression was reduced upon endothelial differentiation;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16008511

Selventa

RA7iNVgwKD3Dnol3JmLMBoEI7CSEgy0KmpNw0UJNQbFpc
has assertion: bp(GO:"cell differentiation") -| r(MGI:Klhdc2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.753+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"cell differentiation") -| r(MGI:Klhdc2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16008511

3
value: we identified three conserved but uncharacterized genes encoding bromodomain containing 3 (BRD3), protein lysine methyltransferase (PLM), and kelch domain containing 2 (KLHDC2), which were downregulated during endothelial differentiation. An RNA blot study showed that these genes were markedly expressed in undifferentiated ES cells, whereas the expression was reduced upon endothelial differentiation;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16008511

Selventa

RAyA9K7QxssxcjLa3eBQdIE8rpdf3w S9RuPZK5RAPXbc
has assertion: p(MGI:Nmu) -> bp(GO:"cellular extravasation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.755+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Nmu) -> bp(GO:"cellular extravasation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16009716

3
value: Moreover, intraplantar injection of NMU into paws induced early inflammatory responses such as mast cell degranulation, vasodilation, and plasma extravasation in WT mice but not in WBB6F(1)-W/W(v) mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16009716

Selventa

RA3wHbs794foy1j AM3CROn-QSe1teHxGkxj 391bt7jw
has assertion: tscript(p(HGNC:EGR4)) -> r(HGNC:ICAM1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.758+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:EGR4)) -> r(HGNC:ICAM1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014385

5
value: EGR-p65 complexes strongly activated transcription of the promoters of the human genes encoding the cytokines interleukin 2, tissue necrosis factor alpha and ICAM-1. The EGR-p65 complexes increased reporter-gene activity about 100-fold and thus exceeded the transcriptional activities of the p65 homodimer and the p65/p50 heterodimers.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014385

Selventa

RA9cHhGiwWpG0y7ouHvoldR4aNJCBAHwM1V0Y6VP871PA
has assertion: path(SDIS:"viral infection") -> r(HGNC:FGG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.765+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:FGG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RAx9HOWyYY9OsJfkb3DHfq4GUscWD0Mn5XHnwTWm1uiE8
has assertion: path(SDIS:"viral infection") -> r(HGNC:FGL1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.769+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:FGL1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RA9Y4Al JoJmTMnMn9weMPp4oHiFhxsaOUEfUto2v46Kg
has assertion: path(SDIS:"viral infection") -> r(HGNC:FXYD2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.771+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:FXYD2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RA7AYG0xtezlOIcF72CBvaKRctdSGeERI98LNFjOjVvNE
has assertion: path(SDIS:"viral infection") -> r(HGNC:S100P)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.781+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:S100P)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RAxG3A8chWyiTtHMpKsu5MMoREiHvaLchcwQvmcGMSsNg
has assertion: path(SDIS:"viral infection") -> r(HGNC:TM4SF20)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.786+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:TM4SF20)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RA7KBr9i93OpYjpJhvn4cvBnTzS90FyLAiC7sUOqLCgDo
has assertion: path(SDIS:"viral infection") -> r(HGNC:UPK1B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.793+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:UPK1B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RA2Is7gaSDcP8VhIyaQvFukJ0QFnaACRnx4NVM-MBldAc
has assertion: path(SDIS:"viral infection") -> r(HGNC:VCAN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.799+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -> r(HGNC:VCAN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16014971

3
value: TABLE 1. Increase in the mRNA levels of fibrinogen and fibrinogen-related genes, as well as other cellular genes, in 3a-expressing stable A549 cell lines, clones U1 and U2, as determined by oligonucleotide microarray analysis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16014971

Selventa

RA4u7zqjbngAKw2Sq2invNnFei8CvXPjB0FLQQ88hgRdc
has assertion: p(MGI:Taf4a) -| r(MGI:Ifit1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.808+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Taf4a) -| r(MGI:Ifit1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16015375

4
value: Figure 5 Changes in gene expression in taf4-/- cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16015375

Selventa

RA3kykL79-pxRZK8FH16fD15IDC6Wg3e66N5RcAevt3OQ
has assertion: p(MGI:Taf4a) -| r(MGI:Thbs1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.818+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Taf4a) -| r(MGI:Thbs1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16015375

4
value: Figure 5 Changes in gene expression in taf4-/- cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16015375

Selventa

RA9voCHfn1kPXPaBzL4lwNPZa4a-zz3wmhjTGB1V7CjSk
has assertion: kin(p(PFR:"MAPK Erk1/3 Family")) -> r(RGD:Tgfb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.822+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"MAPK Erk1/3 Family")) -> r(RGD:Tgfb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16019429

5
value: We show that PDGF-BB induces TSP-1 and TGF-beta1 via the src kinase pathway whereas TNF-a utilizes the MAPK/Erk pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16019429

Selventa

RA1JJXFHfZA-PPmhaOVotb38Q0FVDQ2uZEj GN15CUqIA
has assertion: cat(p(HGNC:CMA1)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.825+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:CMA1)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020275

4
value: RESULTS: Most of the cells in the incubation with chymase were detached by 24 hr. However, chymase-mediated apoptosis was a slower process and was only detected after incubation of cells with chymase for 36 to 48 hr.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020275

Selventa

RA6hHx7 j8DH9bJrpbQavWVAxnVb-Q4aTJbuuZ6rc00d0
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| cat(p(HGNC:ACACA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.826+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| cat(p(HGNC:ACACA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020439

5
value: Activation of AMPK leads to phosphorylation, and thus inhibition, of acetyl coenzyme A carboxylase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020439

Selventa

RA39-492sH1Wis96iSseQDxTVEBVAvuYdZcZBXbBTjJi8
has assertion: p(RGD:Tnf) -| bp(GO:"glucose import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.835+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Tnf) -| bp(GO:"glucose import")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020439

3
value: Although extensively studied in cachexia, autoimmune disease, rheumatoid arthritis, sepsis, and other inflammatory disorders, the role of TNF-alpha and its association with obesity and diabetes is less understood. Infusion of TNF-alpha in rats impaired insulin-stimulated whole body glucose disposal (43).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020439

Selventa

RA0n7mx3jupRGuxmJMc-531raD aB7x90YSTdP1HrzfPE
has assertion: p(HGNC:IL6) -| (p(HGNC:IRS1,pmod(P,Y)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.837+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL6) -| (p(HGNC:IRS1,pmod(P,Y)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex")))
label: p(HGNC:IRS1,pmod(P,Y)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020439

6
value: Although the exact mechanism of resistin function has yet to be identified, Steppan et al. (100) observed increased circulating resistin levels in diet-induced and genetic models of obesity. Inhibition of resistin in these models restored insulin action, whereas administration of resistin inhibited insulin action in control animals. Surprisingly, the evidence linking resistin to diabetes and obesity in humans is less clear. Serum content of resistin is unaffected by obesity and insulin resistance in humans (37). Lee et al. (66) compared BMI, fat mass, and insulin action to resistin levels in 243 subjects (male and female) and observed no relationship. There was also no difference in resistin between lean and obese insulin-resistant subjects. Serum resistin can be elevated in Type 2 diabetes patients, but there was no relationship between adiposity and insulin (70), whereas others have reported no difference in obese, obese diabetic, and nonobese subjects (37). Although there are conflicting reports as to the relationship of resistin to adiposity (5), most investigations agree that resistin is not related to insulin resistance (107). To date, there is no information on the interaction between exercise and resistin. Because the role of resistin in regulating insulin action is unclear at this time, there appears to be little rationale to investigate the influence of exercise on this particular adipocytokine. Interleukin (IL-6). IL-6 is a multifunctional cytokine secreted by numerous cell types including immune cells, skeletal muscle, and adipose tissue. In an effort to determine function, Kim et al. (58) pretreated mice with IL-6 before a hyperinsulinemic- euglycemic clamp. IL-6 blunted skeletal muscle glucose disposal as well as IRS-1-associated phosphatidylinositol 3-kinase activity (58).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020439

Selventa

RA7VNioNHma1yNrtJf02-OrRaBGXQAXxNyv13GGB0sH6k
has assertion: a(SCHEM:"serum insulin") -> path(SDIS:"muscle glucose import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.839+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -> path(SDIS:"muscle glucose import")
label: p(HGNC:IL6) -| (a(SCHEM:"serum insulin") -> path(SDIS:"muscle glucose import"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020439

4
value: Although the exact mechanism of resistin function has yet to be identified, Steppan et al. (100) observed increased circulating resistin levels in diet-induced and genetic models of obesity. Inhibition of resistin in these models restored insulin action, whereas administration of resistin inhibited insulin action in control animals. Surprisingly, the evidence linking resistin to diabetes and obesity in humans is less clear. Serum content of resistin is unaffected by obesity and insulin resistance in humans (37). Lee et al. (66) compared BMI, fat mass, and insulin action to resistin levels in 243 subjects (male and female) and observed no relationship. There was also no difference in resistin between lean and obese insulin-resistant subjects. Serum resistin can be elevated in Type 2 diabetes patients, but there was no relationship between adiposity and insulin (70), whereas others have reported no difference in obese, obese diabetic, and nonobese subjects (37). Although there are conflicting reports as to the relationship of resistin to adiposity (5), most investigations agree that resistin is not related to insulin resistance (107). To date, there is no information on the interaction between exercise and resistin. Because the role of resistin in regulating insulin action is unclear at this time, there appears to be little rationale to investigate the influence of exercise on this particular adipocytokine. Interleukin (IL-6). IL-6 is a multifunctional cytokine secreted by numerous cell types including immune cells, skeletal muscle, and adipose tissue. In an effort to determine function, Kim et al. (58) pretreated mice with IL-6 before a hyperinsulinemic- euglycemic clamp. IL-6 blunted skeletal muscle glucose disposal as well as IRS-1-associated phosphatidylinositol 3-kinase activity (58).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020439

Selventa

RA-btdlFYYqsKsAboyL9cwkhM qp3qtBkxkuR7J1wtxlA
has assertion: a(SCHEM:Diacylglycerol) -> kin(p(HGNC:PRKCE))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.845+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Diacylglycerol) -> kin(p(HGNC:PRKCE))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16020439

4
value: TNF-alpha mediates insulin resistance via serine phosphorylation of insulin receptor substrate (IRS-1) in skeletal muscle, which inhibits the ability of insulin to stimulate GLUT-4 translocation to the cell membrane and therefore reduces glucose uptake (43). Conversely, inhibition of TNF-alpha results in increased insulin-stimulated IRS-1 tyrosine phosphorylation (10, 43). The ability of TNF-alpha to serine phosphorylate IRS-1 may be mediated via diacylglycerol (DAG). Incubating intact rat skeletal muscle strips with TNF-alpha significantly increased palmitate incorporation into DAG (7). This is important because DAGs are known activators of conventional and novel protein kinase C isoforms that serine phosphorylate, and thus inhibit, IRS-1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16020439

Selventa

RA x4OVh4waISEKmr3YR-j8JiCsYAkPCTPdPEbaPZqKZA
has assertion: complex(p(PFH:"NOTCH Family"),p(HGNC:RBPJ)) -> tscript(p(PFH:"NOTCH Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.857+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(PFH:"NOTCH Family"),p(HGNC:RBPJ)) -> tscript(p(PFH:"NOTCH Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16023591

7
value: Jagged1 on tumor cells binds to Notch receptor(s) on endothelial cells. Upon ligand binding, the Notch intracellular domain (NICD) is released from the endothelial cell plasma membrane by the secretase-dependent proteolytic cleavages of Notch receptor. The NICD then translocates to the nucleus, where it interacts with the CSL (named for mammalian CBF1/RBP, Drosophila Su(H), and C. elegans Lag-1) transcription repressor to activate the transcription of target genes.The basic-helix-loop-helix proteins (bHLH) Hairy/Enhancer of Split (Hes1, -5, and -7) and Hes-related proteins (Hey1, -2, and -L) are the best-characterized downstream targets.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16023591

Selventa

RAxaLym-bWTo xu5QeapR4BRxu1ecSjKJg5mMgj g4ZdA
has assertion: tscript(p(PFH:"NOTCH Family")) -> r(HGNC:HEY2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.866+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(PFH:"NOTCH Family")) -> r(HGNC:HEY2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16023591

5
value: Jagged1 on tumor cells binds to Notch receptor(s) on endothelial cells. Upon ligand binding, the Notch intracellular domain (NICD) is released from the endothelial cell plasma membrane by the secretase-dependent proteolytic cleavages of Notch receptor. The NICD then translocates to the nucleus, where it interacts with the CSL (named for mammalian CBF1/RBP, Drosophila Su(H), and C. elegans Lag-1) transcription repressor to activate the transcription of target genes.The basic-helix-loop-helix proteins (bHLH) Hairy/Enhancer of Split (Hes1, -5, and -7) and Hes-related proteins (Hey1, -2, and -L) are the best-characterized downstream targets.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16023591

Selventa

RA85XRTfcKsDXAKHhgJR80UZOpUEqxXIKoINvdiA8xSKA
has assertion: sec(p(HGNC:HGF)) -> kin(p(PFH:"MAPK Erk1/3 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.870+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

sec(p(HGNC:HGF)) -> kin(p(PFH:"MAPK Erk1/3 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16023591

6
value: The tumor associated growth factors HGF, EGF, and TGFA, produced by tumor cells and or stromal cells, induce Jagged1 expression in tumor cells probably in endothelial cells as well through MAPK pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16023591

Selventa

RAymTk0-rwABebyHv3nwE2dx5jGfzL8x8ZGVc08xBtWMA
has assertion: cat(p(HGNC:FTH1)) -| a(CHEBI:"reactive oxygen species")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.882+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:FTH1)) -| a(CHEBI:"reactive oxygen species")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16024802

4
value: when H-ferritin is expressed in L929 cells under a TNF-inducible system, the TNF-induced LIP and subsequent ROS production and cell death were all prevented
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16024802

Selventa

RAyTFuNGSjUx8WC5GuWMItXJ1bdG8Rl7P1b4Uf9YMeQcs
has assertion: cat(p(HGNC:FTH1)) -| bp(GO:"cell death")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.884+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:FTH1)) -| bp(GO:"cell death")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16024802

4
value: when H-ferritin is expressed in L929 cells under a TNF-inducible system, the TNF-induced LIP and subsequent ROS production and cell death were all prevented
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16024802

Selventa

RAzWG5obPpKOnZrePt 70pfpGFEeL-9BkXq8qP3 Ur4mo
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:PFKFB4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.888+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:PFKFB4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16025159

3
value: Our studies clearly demonstrated that PFKFB4 mRNA is also expressed in mammary gland malignant cells (MCF-7 and T47D cell lines) in normoxic conditions and that hypoxia strongly induces it expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16025159

Selventa

RA5GwYN RHZpuAYWKuV7aIU08CRrtTMh27ndZczlUHgME
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:LEP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:LEP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

3
value: Indeed, the proportion of cardiac output that goes to adipose tissue is decreased in obesity, and the obese do not show the post-prandial increase in blood flow which occurs in lean individuals (Karpe et al. 2002). Activation of a transcription factor, hypoxia inducible factor-1 (HIF-1), through the stimulation of the expression of the HIF-1a subunit - the molecular sensor of hypoxia (Semenza 2001, Wenger 2002, Hopfl et al. 2004) - may be the mechanism through which low oxygen tension links to inflammation (Trayhurn & Wood 2004). The target genes for HIF-1 include VEGF and leptin, and expression of both of these has been shown to be stimulated in 3T3-L1 adipocytes in response to hypoxia (Lolmede et al. 2003).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RAyzUOzCEvlnkwRHPH2gi9vPXcIznCSFTGq0M48TDIzcc
has assertion: p(HGNC:NAMPT) -> kin(p(HGNC:INSR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.895+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NAMPT) -> kin(p(HGNC:INSR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

5
value: It was previously identified as pre-B cell colony-enhancing factor (PBEF), a 52 000 mol. wt cytokine expressed in lymphocytes, and importantly it appears to be an insulin mimetic, both binding to and activating the insulin receptor (Fukuhara et al. 2005).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RA9qsUVbIpJUyLb12N59n6RTNvZdKBNhT6nKwE416LexQ
has assertion: cat(p(HGNC:AZGP1)) -> cat(p(HGNC:ADRB3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.901+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AZGP1)) -> cat(p(HGNC:ADRB3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

6
value: Such an action is not only surprising in itself, but also in relation to the augmented expression in visceral adipose tissue given the particular association between this fat depot and the metabolic syndrome. Zinc-a2-glycoprotein, the third novel adipokine, is a 43 000 mol. wt glycoprotein which is synthesized by certain malignant tumours and which has been used as a marker for cancer. The protein stimulates lipid loss in cachexia, and this occurs through the activation of lipolysis (Hirai et al. 1998, Todorov et al. 1998, Sanchez et al. 1999) via b3-adrenoceptors (Russell et al. 2002).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RAxEllUiEv0KpOwcz6r6cCyj2Kotq3gn9q2XfBXds-Scg
has assertion: bp(GO:"response to cold") -| r(HGNC:LEP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.905+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to cold") -| r(HGNC:LEP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

3
value: There have been few reports on the effects of either acute or chronic cold exposure on adipokine production, but substantial changes would be predicted, not least because of the sympathetic activation in WAT. One of the earliest studies on leptin showed that acute exposure of mice to the cold induced a major suppression of ob gene expression in WAT (Trayhurn et al.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RAxw5iuqyhnEj7d0KfHuISfRQNDQTDZjIJB9xatwHadXc
has assertion: bp(GO:"inflammatory response") -> sec(p(HGNC:NGF))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.909+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"inflammatory response") -> sec(p(HGNC:NGF))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

4
value: This suggests that NGF is an inflammatory response protein in adipocytes, a view supported by the subsequent observation that NGF secretion by 3T3-L1 cells is dramatically upregulated by prostaglandin PGD2 and by the J series prostaglandins, PGJ2 and D12-PGJ2 (Bullo et al. 2005).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RA1LEQBGhZOJbjk4vkeiTJWo8a159vtr53juPjxkKdu5g
has assertion: bp(MESHPP:Obesity) positiveCorrelation sec(p(HGNC:NAMPT))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.910+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation sec(p(HGNC:NAMPT))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

4
value: Visfatin is especially intriguing in that this adipokine is highly enriched in visceral fat, in both animals and humans, and its circulating levels are also increased in obesity (Fukuhara et al. 2005).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RA3isaFTvpPIcyMz9nu8ES2gra95ERUigGQKMNC8rWQ-o
has assertion: bp(MESHPP:Obesity) positiveCorrelation sec(p(HGNC:APLN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.914+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation sec(p(HGNC:APLN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026420

4
value: and has now been found to be secreted from adipocytes (Boucher et al. 2005). It is synthesized as a 77 amino acid preproprotein, which is cleaved to a 55 amino acid product and then to further products, the biologically active form apparently being apelin-36 (Tatemoto et al. 1998). Apelin expression and circulating levels are increased in hyperinsulinaemia-associated obesities, including in humans, and in cell culture its expression rises after adipocyte differentiation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026420

Selventa

RA9orO65WVqSIL35Wlpl k47d87NgrhGG qWvjqDKTuNQ
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.919+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> kin(p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026642

5
value: Co-transfection of Akt (myc-Akt) and ASK1 induced a high level of ASK1 phosphorylation, which was decreased approximately 40% by either the phosphoinositide 3-kinase inhibitor LY294002 or cotransfection of ASK1 with a kinase-dead Akt construct (myc-AktKD), suggesting that Akt phosphorylates ASK1 in cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026642

Selventa

RA6jp2g7q1ECOVqWwnX0I-j4PW6mBUFTwujCmhTpUrsBM
has assertion: p(EGID:122953) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.920+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:122953) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16026868

3
value: Specific depletion of JDP2 resulted in p53-independent cell death that resembles apoptosis and was evident at 72 h.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16026868

Selventa

RA9c6vEINQtM62C7dxla0rfr7397QVB9asDIseZnQ5QQs
has assertion: cat(p(RGD:Adrb3)) -| a(SCHEM:Triacylglycerol)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.923+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Adrb3)) -| a(SCHEM:Triacylglycerol)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16027000

4
value: KTO-7924 for 28 days significantly decreased RP WAT weight, plasma triglyceride, free fatty acid, and insulin, and improved insulin resistance
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16027000

Selventa

RAyu1ojMytBnbgVg1w1sdfTAURj8aTzglNbOFqW5KAFoU
has assertion: cat(p(RGD:Adrb3)) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.924+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Adrb3)) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16027000

4
value: KTO-7924 for 28 days significantly decreased RP WAT weight, plasma triglyceride, free fatty acid, and insulin, and improved insulin resistance
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16027000

Selventa

RA95ooeVNQ26SiPlT7hNk9FVfgT3OnBRByHWrpvOYiemg
has assertion: cat(p(RGD:Adrb3)) -| a(SCHEM:"serum triacylglycerol")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.928+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Adrb3)) -| a(SCHEM:"serum triacylglycerol")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16027000

4
value: KTO-7924 for 28 days significantly decreased RP WAT weight, plasma triglyceride, free fatty acid, and insulin, and improved insulin resistance
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16027000

Selventa

RA7vkwYJrrHt8ZggbAnt3GIpEn1vyqzNRjCiZT7hooiJE
has assertion: kin(p(PFR:"Akt Family")) -> p(RGD:Vcp,pmod(P,S,352))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.937+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Akt Family")) -> p(RGD:Vcp,pmod(P,S,352))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16027165

5
value: significant increase in Akt activation in rat CA1 hippocampal region extracts Active recombinant Akt phosphorylated recombinant VCP in vitro. Site-directed mutagenesis studies identified Ser352, Ser746, and Ser748 as Akt phosphorylation sites on VCP.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16027165

Selventa

RA JKenY2QSMwSXPyEZmcIRWTGNg3owpFrC6X1Lgm2PkU
has assertion: a(SCHEM:Thiazolidinedione) -> r(RGD:Serpina12)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.948+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Thiazolidinedione) -> r(RGD:Serpina12)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16030142

3
value: Recently, there has been a worldwide increase in the incidence of obesity associated with a metabolic syndrome known as type 2 diabetes, the development of which seems to be as a result of high-caloric diet intake and physical inactivity (1, 2); and predicted estimates suggest that the population with this syndrome may double to ~300 million by the year 2025 (3). One of the critical determinants for the development of this obesity may be an increase in the regional distribution of body fat, i.e., abdominal obesity. The latter often shows clustering of atherogenic risk factors (4, 5), i.e., hypertension, dyslipidemia, alterations in coagulation and inflammatory cytokine profiles, and hyperinsulinemic insulin resistance. As a consequence, there is an expected increase in morbidity and mortality of cardiovascular disease (6-9). Vigorous efforts have been made to delineate the relationship between increased adiposity and insulin resistance. In this regard, some molecules, including free fatty acids, leptin (10, 11), TNF-alpha (12, 13), acylation-stimulating protein (14, 15), adiponectin (16, 17), and resistin (18), which are secreted by the adipocytes, may modulate the sensitivity of insulin, the action of which activates multiple signaling events after phosphorylation of insulin receptor and several other molecules in type 2 diabetes (19, 20). To address the causal relationship between insulin resistance and obesity, various animal models, e.g., Otsuka Long-Evans Tokushima fatty (OLETF) rats, have been used by many investigators. The OLETF rat is an animal model of type 2 diabetes, which is characterized by abdominal obesity, insulin resistance, hypertension, and dyslipidemia (21). Previously, we isolated a ~135-bp cDNA fragment during differential screening of the genes upregulated in visceral adipose tissues of obese OLETF rats and down-regulated in nonobese and diabetes-resistant Long-Evans Tokushima Otsuka (LETO) rats (22). This cDNA fragment exhibited partial homo[cell cut: 3950 characters, first 2000 kept]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16030142

Selventa

RA2UdCmDB0f1cr3NyhLMhr9HxC2LST6EOA3CXfj1xf5GY
has assertion: a(SCHEM:"serum insulin") -> r(RGD:Serpina12)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.951+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -> r(RGD:Serpina12)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16030142

3
value: at 30 wk of age and maintained its levels up to 50 wk, while reducing in visceral WATs, i.e., retroperitoneal and MES fat (Fig. 2E). Similarly, insulin therapy up-regulated expression of vaspin in SUB WATs along with a partial reduction in visceral WATs at 30 wk of age.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16030142

Selventa

RA2r3aFmJt1g-lrF7yDhAkCAhY5N-2FtZvPdkDeOJTPM8
has assertion: a(SCHEM:"serum insulin") -> kin(complex(NCM:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.960+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -> kin(complex(NCM:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034410

3
value: Fenretinide treatment did not affect food intake, body weight or the development of obesity on the high-fat diet (not shown). Mice on a high-fat diet developed marked insulin resistance (Fig. 4d) and glucose intolerance (Fig. 4e). Fenretinide treatment improved insulin sensitivity (Fig. 4d) and normalized glucose tolerance (Fig. 4e). Similar results were obtained in ob/ob mice treated with fenretinide (not shown). Thus, both genetic and pharmacological interventions that decrease serum RBP4 levels improve insulin sensitivity. RBP4 impairs insulin signalling in muscle To understand how RBP4 alters insulin sensitivity, we studied insulin signalling in muscle and liver of Rbp4-/- mice and mice overexpressing human RBP4 (RBP4-Tg mice). Basal phosphoinositide 3-kinase (PI(3)K) activity was similar in all genotypes (Fig. 5a-d). Insulin resulted in a 26-fold increase in PI(3)K activity in muscle of control mice, but its effect was reduced by 30% in RBP4-Tg mice (Fig. 5a).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034410

Selventa

RA6z9I2lQBRqjCw SqOs6kdBxnlAw1ZYMKQUfhpQYtHY0
has assertion: p(MGI:Rbp4) -> a(SCHEM:"serum insulin")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.964+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Rbp4) -> a(SCHEM:"serum insulin")
label: path(SDIS:"food intake") -> (p(MGI:Rbp4) -> a(SCHEM:"serum insulin"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034410

4
value: Rosiglitazone treatment also completely normalized the elevated serum RBP4 levels in adipose-Glut4-/- mice (Fig. 2c). The dramatic effect of this insulin-sensitizing anti-diabetic agent on serum RBP4 levels raises the possibility that elevation of RBP4 might play a causative role in insulin resistance and type 2 diabetes. Increased RBP4 causes insulin resistance Transgenic mice expressing human RBP4 driven by the mouse muscle creatine kinase (Mck) promoter (RBP4-Tg) have an ,3-fold increase in serum RBP4 levels compared with non-transgenic mice19, similar to the elevation observed in serum of adipose-Glut4-/- mice (see Supplementary Fig. 2). RBP4-Tg mice develop normally. Growth curves are similar to wild-type mice until at least 16 weeks of age (not shown). Insulin levels are higher in fed RBP4-Tg mice compared with wild-type mice, indicating insulin resistance (see Supplementary Table 2), which is also evident in insulin tolerance tests (Fig. 3a). There are no differences in glucose, free fatty acid, leptin, adiponectin or resistin levels in fed RBP4-Tg mice compared with controls (see Supplementary Table 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034410

Selventa

RA0X1j5ojmcuvsJcustCeC5PedGviZSh50aStur7qhLdY
has assertion: p(MGI:Slc2a4) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.967+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Slc2a4) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034410

3
value: There was no difference in the magnitude of serum RBP4 elevation between the obese and obese-diabetic groups, suggesting that obesity and insulin resistance, but not hyperglycaemia, are associated with elevated serum RBP4 in humans. Rosiglitazone reverses RBP4 elevation The anti-diabetic agent rosiglitazone is a peroxisome proliferator activated receptor-gamma (PPARg) agonist that improves insulin sensitivity17. Treatment of adipose-Glut4-/- mice with rosiglitazone for three weeks completely reversed their insulin resistance and glucose intolerance18.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034410

Selventa

RA67h wWKqTCZhPnNQ2BPqFk5IcbZ9oGu9LdyPh6LkY8c
has assertion: a(CHEBI:aldosterone) -> bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.969+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:aldosterone) -> bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034720

2
value: Aldosterone dose-dependently inhibited expression of uncoupling protein-1 (UCP-1) by 30% (p dose-dependently impaired insulin-induced glucose uptake by about 25% (p 0.01).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034720

Selventa

RA45EqI2mrnTOdtLjyT40irUVi-0qodTVe SpZH6Sh1aQ
has assertion: a(CHEBI:aldosterone) -> bp(GO:"inflammatory response")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.971+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:aldosterone) -> bp(GO:"inflammatory response")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034720

2
value: On a transcriptional level, mRNA of the proinflammatory adipokines leptin and monocyte chemoattractant protein-1 (MCP-1) was increased by 5,000% and 40%, respectively, by aldosterone exposure (p demonstrates that aldosterone directly impacts on major adipose functions including stimulation of proinflammatory adipokines.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034720

Selventa

RA8itEomgfM3v-oB4IMDVMZAarTiM9kfWA7-PjD2HKCxY
has assertion: a(CHEBI:aldosterone) -> r(MGI:Lep)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.974+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:aldosterone) -> r(MGI:Lep)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16034720

3
value: On a transcriptional level, mRNA of the proinflammatory adipokines leptin and monocyte chemoattractant protein-1 (MCP-1) was increased by 5,000% and 40%, respectively, by aldosterone exposure (p demonstrates that aldosterone directly impacts on major adipose functions including stimulation of proinflammatory adipokines.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16034720

Selventa

RA97f9dVhusGui2UHLyd3xhtvRpdnXySpSW1ZRlfBmhxo
has assertion: kin(p(HGNC:MAPK1)) => p(HGNC:GSK3B,pmod(P,T,43))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.981+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK1)) => p(HGNC:GSK3B,pmod(P,T,43))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16039586

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16039586

Selventa

RA55dJf-Pv2Ste3Ve-UNGejmd2Axe-yBe zODaVew1prc
has assertion: kin(p(HGNC:MAPK3)) => p(HGNC:GSK3B,pmod(P,T,43))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.982+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) => p(HGNC:GSK3B,pmod(P,T,43))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16039586

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16039586

Selventa

RA8Wj9IIx89GDH6b9teK-Hn4eHGJVn8MEAFEnxVlB83vo
has assertion: phos(p(HGNC:PTPMT1)) -> sec(p(EGID:3630))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.984+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPMT1)) -> sec(p(EGID:3630))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16039589

6
value: Knockdown of PTPMT1 expression in the pancreatic insulinoma cell line INS-1 832/13 alters the mitochondrial phosphoprotein profile and markedly enhances both ATP production and insulin secretion.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16039589

Selventa

RA9Vth85-kJ76EUhnJq5tQtSOTSceFUR2h9XsY5oCYndY
has assertion: kin(p(HGNC:MAP3K3)) => kin(p(HGNC:MAP2K1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.988+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K3)) => kin(p(HGNC:MAP2K1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16039990

6
value: from Gene MAP3K3: This gene product is a 626-amino acid polypeptide that is 96.5% identical to mouse Mekk3. Its catalytic domain is closely related to those of several other kinases, including mouse Mekk2, tobacco NPK, and yeast Ste11. Northern blot analysis revealed a 4.6-kb transcript that appears to be ubiquitously expressed. This protein directly regulates the stress-activated protein kinase (SAPK) and extracellular signal-regulated protein kinase (ERK) pathways by activating SEK and MEK1/2 respectively; it does not regulate the p38 pathway. In cotransfection assays, it enhanced transcription from a nuclear factor kappa-B (NFKB)-dependent reporter gene, consistent with a role in the SAPK pathway. Alternatively spliced transcript variants encoding distinct isoforms have been observed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16039990

Selventa

RA6jVj32XvwNb3-yaJi6wHZxsFkO8RzMa685iCCuBf7lo
has assertion: kin(p(HGNC:MAP3K3)) -> kin(p(HGNC:MAPK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:36.994+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K3)) -> kin(p(HGNC:MAPK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16039990

6
value: hKSR-2 also regulates the activity of MEKK3 (another MAP3K family member) in HEK-293T cells. We demonstrate that hKSR-2 is a negative regulator of MEKK3-mediated activation of MAP kinase (specifically ERK and JNK) and NF-kappaB pathways, and concurrently inhibits MEKK3-mediated interleukin-8 production.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16039990

Selventa

RA59T3mLsvI3-NZ3PYCG2IfBz0GR40WO H7WiqB8UDkgM
has assertion: p(HGNC:RB1CC1) -> bp(GO:"cell growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.005+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:RB1CC1) -> bp(GO:"cell growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16043512

3
value: We found that association of FIP200 with the TSC1-TSC2 complex correlated with its ability to increase cell size and up-regulate S6 kinase phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16043512

Selventa

RA3-Tu-Ht62Yz5 1 TOhp52GRjBB69vCox0duLJaJ1eTc
has assertion: complex(p(HGNC:RB1CC1),p(HGNC:TSC1),p(HGNC:TSC2)) -> bp(GO:"cell growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.010+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:RB1CC1),p(HGNC:TSC1),p(HGNC:TSC2)) -> bp(GO:"cell growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16043512

6
value: We found that association of FIP200 with the TSC1-TSC2 complex correlated with its ability to increase cell size and up-regulate S6 kinase phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16043512

Selventa

RA4MONzgjCAIk9a157MdmfM1hzzfOaEgw5IqwWs9HAyaE
has assertion: a(SCHEM:"Advanced Glycation End Product") -> a(SCHEM:"serum glucose")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.011+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Advanced Glycation End Product") -> a(SCHEM:"serum glucose")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16046296

2
value: 75% of HAGE-HF mice were diabetic and exhibited higher body weight (P< 0.001), fasting glucose (P < 0.001), insulin (P< 0.001), and serum AGEs (P < 0.01) than control mice, while none of the LAGE-HF mice were diabetic despite a similar rise in body weight and plasma lipids.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16046296

Selventa

RA1Nzgukt-e4Y0uLvLWafz5k-MzRtgWujVyc-H4W83aw0
has assertion: cat(p(MGI:Dgat1)) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.033+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Dgat1)) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16054046

4
value: ... improved insulin sensitivity in the face of moderate obesity that is observed in transgenic mice overexpressing DGAT in adipose tisuue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16054046

Selventa

RA4wmyThhHQyFAQp3kRjNFkbGqh6hU7YFzBLokXx8W0mc
has assertion: a(CHEBI:fulvestrant) -| r(HGNC:SOCS3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.039+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:fulvestrant) -| r(HGNC:SOCS3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055089

3
value: The suppressor of cytokine signalling (SOCS) protein family negatively regulates cytokine action. In this study, we investigated the effects of estrogen (E2) on SOCS-3 expression in T47D and MCF-7 human breast cancer cells. Real-time PCR analysis of E2-treated T47D cells revealed a ligand and time-dependent increase in of SOCS-3 mRNA levels. Cloning of a 1.7 kb fragment of the human SOCS-3 5' flanking sequence, and subsequent analysis of potential transcription factor-binding sites identified an incomplete ERE motif located -1493 to -1489 upstream of the start site. Transient transfection of the cloned fragment in MCF-7 cells showed that both E2 and genistein treatment caused an increase in reporter gene activity, which was inhibited by co-treatment with ICI 182,780. Chromatin immunoprecipitation analysis revealed an E2 and time-dependent recruitment of ERalpha to the E2 responsive region of the human SOCS-3 promoter. In summary, this study shows that ERalpha directly regulates human SOCS-3 promoter activity in human breast cancer cells, thus modulating cytokine activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055089

Selventa

RA3YJDzV8V8VaxGwLoGZtakeY1q4R92SPwMiOO BE2H5g
has assertion: a(SCHEM:"cyclic AMP") -| p(HGNC:CFL1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.043+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -| p(HGNC:CFL1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055445

3
value: . Pretreatment of cultures with tautomycin, a protein phosphatase type 1 inhibitor, blocked the effect of cAMP on 1) the dephosphorylation of cofilin, 2) the decrease in RLC phosphorylation, and 3) the decrease in isometric tension.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055445

Selventa

RAxC4hMd3ui7DFK1hf3mZWbSKAeY5tJr5C6-mH0lSs6cM
has assertion: p(HGNC:SUMO1) -| tscript(complex(NCH:"AP-1 Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.046+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SUMO1) -| tscript(complex(NCH:"AP-1 Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055710

4
value: lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229 sumoylation entails lower AP-1 transactivation activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055710

Selventa

RA9-8tKUqIe7 jpcq--5b4XIhK6 JK5J1KxCV6B7R-N0o
has assertion: p(HGNC:SUMO1) -| tscript(p(HGNC:JUN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.048+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SUMO1) -| tscript(p(HGNC:JUN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055710

5
value: lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229 sumoylation entails lower AP-1 transactivation activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055710

Selventa

RA-rW Uh530jaX-5eZ-KgMPh-1tF9pIlQMHzq1dJN9FjQ
has assertion: p(HGNC:SUMO2) -| tscript(complex(NCH:"AP-1 Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.050+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SUMO2) -| tscript(complex(NCH:"AP-1 Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055710

4
value: lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229 sumoylation entails lower AP-1 transactivation activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055710

Selventa

RA7i7IEXUDD8kFEyLquj ogB-wR5A3nx6fs 9DhHVNjjo
has assertion: p(HGNC:SUMO3) -| tscript(p(HGNC:JUN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.056+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SUMO3) -| tscript(p(HGNC:JUN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16055710

5
value: lysine 265 of c-Fos is conjugated by the peptidic posttranslational modifiers SUMO-1, SUMO-2, and SUMO-3 and that c-Jun can be sumoylated on lysine 257 as well as on the previously described lysine 229 sumoylation entails lower AP-1 transactivation activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16055710

Selventa

RAwtUz4HfvjcqujV4ACGbQhxSxzqslEIZujb-EkOLFzus
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:C1QTNF5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.059+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:C1QTNF5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16059715

3
value: The analyses indicated that the inflammation/immune response category was over-represented, and that most inflammation-related genes were upregulated in adipocytes of obese subjects. Quantitative real-time PCR confirmed the transcriptional upregulation of representative inflammation-related genes (CCL2 and CCL3) encoding the chemokines monocyte chemoattractant protein-1 and macrophage inflammatory protein 1alpha. The differential expression levels of eight positional candidate genes, including inflammation-related THY1 and C1QTNF5,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16059715

Selventa

RAxS64Sr6-P6PMa5VT1K AoRGUIFxwCGhI X2Jsboo5aI
has assertion: tscript(p(HGNC:FOXO3)) -> p(HGNC:TNFSF10)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.065+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:FOXO3)) -> p(HGNC:TNFSF10)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061480

5
value: A study found that FOXO3a induces apoptosis in LAPC4 prostate cancer cells via the up-regulation of its direct target tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) (8).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061480

Selventa

RA -InUy0T5WDapONnEXw8 U3G-bh1AgUUazGKM9VH22g
has assertion: tscript(p(MGI:Trp53)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.073+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Trp53)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061649

4
value: In p53-competent cells, Ckap2 does not induce tetraploidy but activates p53-mediated cell cycle arrest and apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061649

Selventa

RAwq4BBTzJaPNZjskIgmVpW4yqDLiSf092Rln etY3U0I
has assertion: p(HGNC:YAP1) => tscript(p(HGNC:TP73))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.124+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:YAP1) => tscript(p(HGNC:TP73))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061658

5
value: Yes-associated protein (YAP), also containing WW domains, was shown to associate with p73 and enhance its transcriptional activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061658

Selventa

RA65iWxkNEEwQ3DFVTcGginONhCMeRSaABxMJOf6oKloY
has assertion: a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.130+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide")
label: cat(p(HGNC:SOD2)) -> (a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061713

5
value: Superoxide dismutases (SODs) are the only enzyme family with activity against superoxide radicals (resulting in hydrogen peroxide production). These enzymes include manganese SOD (MnSOD), copper zinc SOD (CuZnSOD), and extracellular SOD (ECSOD).21?23 All of them are widely expressed in human lung.24 CuZnSOD, which is mainly a cytosolic enzyme, is evenly distributed intracellularly but is also found in the nucleus and lysosomes.25
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061713

Selventa

RA53UKrfcjy6GHBPs2wqIi6HvOHnQ5kpKxolhnKMMG-UE
has assertion: cat(p(HGNC:SOD1)) -> a(CHEBI:"hydrogen peroxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.135+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SOD1)) -> a(CHEBI:"hydrogen peroxide")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061713

4
value: Superoxide dismutases (SODs) are the only enzyme family with activity against superoxide radicals (resulting in hydrogen peroxide production). These enzymes include manganese SOD (MnSOD), copper zinc SOD (CuZnSOD), and extracellular SOD (ECSOD).21?23 All of them are widely expressed in human lung.24 CuZnSOD, which is mainly a cytosolic enzyme, is evenly distributed intracellularly but is also found in the nucleus and lysosomes.25
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061713

Selventa

RAwU46NqoFK9ogJoWUl7MXf8m0oMMgOiVjo3 spTSn6o
has assertion: a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.136+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide")
label: cat(p(HGNC:SOD1)) -> (a(SCHEM:Superoxides) -> a(CHEBI:"hydrogen peroxide"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061713

5
value: Superoxide dismutases (SODs) are the only enzyme family with activity against superoxide radicals (resulting in hydrogen peroxide production). These enzymes include manganese SOD (MnSOD), copper zinc SOD (CuZnSOD), and extracellular SOD (ECSOD).21?23 All of them are widely expressed in human lung.24 CuZnSOD, which is mainly a cytosolic enzyme, is evenly distributed intracellularly but is also found in the nucleus and lysosomes.25
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061713

Selventa

RA ie4b1AV RUqPJqMyjIrDFqDVQI3Rsmv73VA 68QjZo
has assertion: path(SDIS:"acute phase reaction") -| r(HGNC:ACADM)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.143+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"acute phase reaction") -| r(HGNC:ACADM)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061943

3
value: mRNA levels of PGC-1alpha, ERRalpha, and MCAD are markedly reduced in the liver, heart, and kidney of mice during the lipopolysaccharide (LPS)-induced APR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061943

Selventa

RA3s2u6bEPUxvpxgtr46hbkscmxENlywfwNpaUSV lH3U
has assertion: path(SDIS:"acute phase reaction") -| r(HGNC:PPARGC1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.151+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"acute phase reaction") -| r(HGNC:PPARGC1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16061943

3
value: mRNA levels of PGC-1alpha, ERRalpha, and MCAD are markedly reduced in the liver, heart, and kidney of mice during the lipopolysaccharide (LPS)-induced APR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16061943

Selventa

RA51NRGUsvrRBuchYrTt7No4P6kGtnuQOrofVsDl5Yb8A
has assertion: a(CHEBI:glucocorticoid) -> r(RGD:Sftpa1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.159+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:glucocorticoid) -> r(RGD:Sftpa1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/1606951

3
value: S1 mapping of precursor transcripts has confirmed the stimulating effect of glucocorticoids on SP-A rat gene transcription in vivo.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/1606951

Selventa

RAxGaDM-h9fFhKwxUj7mcZkhhS3FkXhomqN5xWB-EfmPs
has assertion: kin(p(MGI:Akt1)) -> bp(GO:angiogenesis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.160+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Akt1)) -> bp(GO:angiogenesis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16075056

4
value: Here we show that the genetic loss of Akt1, but not Akt2, in mice results in defective ischemia and VEGF-induced angiogenesis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16075056

Selventa

RA2iPfFsaoUtTZOGSajCgdfWPpZLP5BvjQjCGxX8EJero
has assertion: p(HGNC:FLT4,pmod(P)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.163+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FLT4,pmod(P)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16076871

4
value: Functional and biochemical anlaysis of the E-R3 chimera also identified the contribution of tyrosines 1230/1231 to VEGFR-3- dependent proliferation, migration and survival. Our data show that these tyrosine residues activate the classic PI3K/AKT and ERK pathways upon GRB2 direct recruitment to the receptor. This site must collaborate with Y1337, which was previously shown to recruit SHC and indirectly GRB2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16076871

Selventa

RA89GeMTOgV3uHjXXHUhuID9Bn-tlQxyxErHFtgZnXvxQ
has assertion: a(CHEBI:dexamethasone) -| (kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.167+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:dexamethasone) -| (kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B)))
label: kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16078016

7
value: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16078016

Selventa

RAw891BrwxeSj4pKQHHnduPY GA7yalJ9qjnhB53Vt3jw
has assertion: a(CHEBI:dexamethasone) -| (kin(p(HGNC:INSR)) -| kin(p(HGNC:GSK3B)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.169+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:dexamethasone) -| (kin(p(HGNC:INSR)) -| kin(p(HGNC:GSK3B)))
label: kin(p(HGNC:INSR)) -| kin(p(HGNC:GSK3B))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16078016

7
value: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16078016

Selventa

RAxxzl1sqaEi9HWmSCcsyo6X2o9Jqhgr8wOjV0GkEmhvw
has assertion: a(CHEBI:dexamethasone) -| (kin(p(MGI:Insr)) -> kin(p(PFM:"Akt Family")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.174+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:dexamethasone) -| (kin(p(MGI:Insr)) -> kin(p(PFM:"Akt Family")))
label: kin(p(MGI:Insr)) -> kin(p(PFM:"Akt Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16078016

7
value: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16078016

Selventa

RA-krc7qZ3rUELTQBbgRvLytf2AzTHqjpUxOiUFnL-WEs
has assertion: kin(p(HGNC:INSR)) -> p(HGNC:GSK3B,pmod(P,S))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.180+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:INSR)) -> p(HGNC:GSK3B,pmod(P,S))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16078016

5
value: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16078016

Selventa

RA5pIYwKxUXnFKrlekJtj0qw-i0exCWrsXVXssLBOUIJs
has assertion: kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.185+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B))
label: tscript(p(HGNC:NR3C1)) -| (kin(p(PFH:"AKT Family")) =| kin(p(HGNC:GSK3B)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16078016

Selventa

9
value: Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16078016

RAyY OBcnMlm2 dXPXk-SqDcMwtj L4LiKUhtJBY8sqeQ
has assertion: a(CHEBI:malathion) -| r(HGNC:BUB1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:malathion) -| r(HGNC:BUB1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16079077

3
value: in response to malathion three genes with increased expression after treatment in all four cell strains. These genes were two aldo-keto reductases (AKR1C1 and AKR1C2) and an estrogen-responsive gene (EBBP). Decreased expression of six RNA species was seen at various time points in all cell strains analyzed: plasminogen activator (PLAT), centromere protein F (CPF), replication factor C (RFC3), thymidylate synthetase (TYMS), a putative mitotic checkpoint kinase (BUB1)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16079077

Selventa

RA7FNolV95OaSpjwb SeKf6YoFRBn6ozIzNV82UhSsZ9M
has assertion: a(CHEBI:malathion) -> r(HGNC:TRIM16)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.202+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:malathion) -> r(HGNC:TRIM16)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16079077

3
value: in response to malathion three genes with increased expression after treatment in all four cell strains. These genes were two aldo-keto reductases (AKR1C1 and AKR1C2) and an estrogen-responsive gene (EBBP). Decreased expression of six RNA species was seen at various time points in all cell strains analyzed: plasminogen activator (PLAT), centromere protein F (CPF), replication factor C (RFC3), thymidylate synthetase (TYMS), a putative mitotic checkpoint kinase (BUB1)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16079077

Selventa

RA0Cr22R4UIGH3-J6iofHCNQRXkWLnVoOmDLOJLDaiqZY
has assertion: p(HGNC:AR) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.206+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AR) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16079795

3
value: Here we show that lysine-specific demethylase 1 (LSD1; also known as BHC110) co-localizes with the androgen receptor in normal human prostate and prostate tumour. LSD1 interacts with androgen receptor in vitro and in vivo, and stimulates androgen-receptor-dependent transcription. Conversely, knockdown of LSD1 protein levels abrogates androgen-induced transcriptional activation and cell proliferation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16079795

Selventa

RA6z526BS0J983EaqDIpAJZxGkfEJABUzdYaZLj5v5d1A
has assertion: a(CHEBI:"hydrogen peroxide") -> p(HGNC:HRAS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"hydrogen peroxide") -> p(HGNC:HRAS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081426

3
value: To this end, we employed 1) PD 98059 and U0126 (2 h and 15 min of incubation, respectively), which inhibit MEK (MAPKK); and 2) a dominant-negative MEK variant that inhibits cellular MEK (see \"Materials and Methods\"). The results, shown in Fig. 3, A-C, demonstrate that induction of Ha-Ras by H2O2 was abolished by MEK inhibition.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081426

Selventa

RAw2lg6O1dWpz8JBnFWJTkb4TfLpzS4HFi2TkgMRTfuII
has assertion: a(CHEBI:ciprofibrate) -| r(HGNC:CSNK1D)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.220+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -| r(HGNC:CSNK1D)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA HHjEOYm7GZNMpeQ6NsdfTGrQoRo 7V3c8JzMuis06U
has assertion: a(CHEBI:ciprofibrate) -| r(HGNC:CYP1A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.221+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -| r(HGNC:CYP1A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA yVHrZzvYaun750a ta7QzzusOS-q1lOmyGkAMoi4Ig
has assertion: a(CHEBI:ciprofibrate) -| r(HGNC:POLD1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.232+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -| r(HGNC:POLD1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA2-eY0haRQGvVZDM3uJfXf9ZhpORCwWCdxlCwQgnbbYU
has assertion: a(CHEBI:ciprofibrate) -| r(HGNC:SMC1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.234+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -| r(HGNC:SMC1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA2VjydcdvgguCBsPrjqP8zX8-aPTbNjIc6H0pyEScd-c
has assertion: a(CHEBI:ciprofibrate) -| r(HGNC:VEGFA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.239+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -| r(HGNC:VEGFA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA1A-6s4uf7R0WUw2scGlP-ILipLKLdeKHj4 Oyy0 6R4
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:APEX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.240+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:APEX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA6XkyNdHArvLQmzuw 9HCPWJ7EH7jJV5aGvPKmup gQc
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:ATOX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.241+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:ATOX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA n7L8ZwEq7U2FnJ1QoZwileGZP5mq mFPgPyEZB5zdg
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:DNAJA1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.248+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:DNAJA1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RAyEBnULf1wVtryjTsDuZeAF3TBMhnJNYuX1dkqhMAdZU
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:EI24)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.250+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:EI24)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RAyVarZhW6Yvz9JQ2X5flz3WIlklzp4FL1e7gylBs1i70
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:NME3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.261+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:NME3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RAzUTxqxmB32cLNH0fttik1Hbwje61Gxtbxd7HmJVt1FA
has assertion: a(CHEBI:ciprofibrate) -> r(HGNC:SHC1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.263+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ciprofibrate) -> r(HGNC:SHC1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081524

3
value: CYNOMOLGUS MONKEYS were exposed to ciprofibrate at various dose levels for either 4 or 15 days, and the liver transcriptional profiles were examined using Affymetrix human GeneChips. Data taken from Supplementary table 4. 27 genes upregulated and 22 genes downregulated. Probesets with p > 0.01 were selected as differentially expressed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081524

Selventa

RA0LOZlT1WaTRTBZE-Daa5jh5kXyOpCZ3nzLV4m2UB1HY
has assertion: a(CHEBI:lipopolysaccharide) -> r(HGNC:G0S2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.277+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(HGNC:G0S2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081831

3
value: LPS stimulates a vigorous inflammatory response from circulating leukocytes that varies greatly from individual to individual. The goal of this study was to use an unbiased approach to identify differences in gene expression that may account for the high degree of interindividual variability in inflammatory responses to LPS in the normal human population. We measured LPS-induced cytokine production ex vivo in whole blood from 102 healthy human subjects and identified individuals who consistently showed either very high or very low responses to LPS (denoted lps(high) and lps(low), respectively). Comparison of gene expression profiles between the lps(high) and lps(low) individuals revealed 80 genes that were differentially expressed in the presence of LPS and 21 genes that were differentially expressed in the absence of LPS (p confirmed using real-time RT-PCR. Functional relevance for one gene confirmed to be expressed at a higher level in lps(high), adipophilin, was inferred when reduction in adipophilin mRNA by small interfering RNA in the human monocyte-like cell line THP-1 resulted in a modest but significant reduction in LPS-induced MCP-1 mRNA expression. These data illustrate a novel approach to the identification of factors that determine interindividual variability in innate immune inflammatory responses and identify adipophilin as a novel potential regulator of LPS-induced MCP-1 production in human monocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081831

Selventa

RA3wkW1s1fCbMvjqTDKfDYRnOW9gZv2bv37Mjia0zViXk
has assertion: a(CHEBI:lipopolysaccharide) -> r(HGNC:IL12B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.278+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(HGNC:IL12B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16081831

3
value: LPS stimulates a vigorous inflammatory response from circulating leukocytes that varies greatly from individual to individual. The goal of this study was to use an unbiased approach to identify differences in gene expression that may account for the high degree of interindividual variability in inflammatory responses to LPS in the normal human population. We measured LPS-induced cytokine production ex vivo in whole blood from 102 healthy human subjects and identified individuals who consistently showed either very high or very low responses to LPS (denoted lps(high) and lps(low), respectively). Comparison of gene expression profiles between the lps(high) and lps(low) individuals revealed 80 genes that were differentially expressed in the presence of LPS and 21 genes that were differentially expressed in the absence of LPS (p confirmed using real-time RT-PCR. Functional relevance for one gene confirmed to be expressed at a higher level in lps(high), adipophilin, was inferred when reduction in adipophilin mRNA by small interfering RNA in the human monocyte-like cell line THP-1 resulted in a modest but significant reduction in LPS-induced MCP-1 mRNA expression. These data illustrate a novel approach to the identification of factors that determine interindividual variability in innate immune inflammatory responses and identify adipophilin as a novel potential regulator of LPS-induced MCP-1 production in human monocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16081831

Selventa

RA5a5t TZ2gRAm9LXRFGdl6iAPRyrmOj4n026IZkf0VbQ
has assertion: p(HGNC:IL13) -> path(SDIS:"tight junction permeability")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.285+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL13) -> path(SDIS:"tight junction permeability")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16083712

3
value: IL-13 had a dose-dependent effect on transepithelial resistance of HT-29/B6 monolayers (reduction to 60% +/- 4%), whereas IL-4 had no effect. This was due to an increased number of apoptotic cells (5.6-fold +/- 0.9-fold) and an increased expression of the pore-forming tight junction protein claudin-2 to 295% +/- 37%, both of which contributed equally. Finally, epithelial restitution velocity decreased from 15.1 +/- 0.6 to 10.6 +/- 0.5 microm/h after treatment with IL-13.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16083712

Selventa

RA7pZrCoM7SB-gXSec56zLFy38AWwF3UuLkow-zyKQ1IY
has assertion: tport(p(HGNC:LDLR)) -| a(SCHEM:"Oxidized Low Density Lipoprotein")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.286+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tport(p(HGNC:LDLR)) -| a(SCHEM:"Oxidized Low Density Lipoprotein")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16083882

4
value: In FH patients, elevation in serum LDL-cholesterol levels secondary to the LDL receptor defect results in the formation of oxidized or otherwise modified LDL, and in their uptake by the macrophage scavenger receptors, leading to massive lipid accumulation and foam cell formation [10].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16083882

Selventa

RA9Ns7MnhWbQFmyIdQNZ0Xc0NENEcyf2IYTjrcznKFyG0
has assertion: p(MGI:Igf1) -> p(MGI:Ccnd1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.297+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Igf1) -> p(MGI:Ccnd1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16086373

4
value: Protein levels of cyclins (D1, E, A), E2F1, and E2F4 were all elevated in the epidermis of BK5.IGF-1 mice. Also, immunoprecipitation experiments demonstrated an increase in cdk4/cyclin D1 and cdk2/cyclin E complex formation,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16086373

Selventa

RA4-uoVe9 G4J2Zur4hYI-Mf0k9UxIbrFu7HYL2GNzRDs
has assertion: p(MGI:Igf1) -> p(MGI:E2f1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.299+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Igf1) -> p(MGI:E2f1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16086373

4
value: Protein levels of cyclins (D1, E, A), E2F1, and E2F4 were all elevated in the epidermis of BK5.IGF-1 mice. Also, immunoprecipitation experiments demonstrated an increase in cdk4/cyclin D1 and cdk2/cyclin E complex formation,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16086373

Selventa

RAzimOnAPqDC8uyhHTBP26pUr9E9e-kKAGCilsN4uZ7kk
has assertion: p(MGI:Igf1) -> p(PFM:"Gsk3 Family",pmod(P,S,9))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.300+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Igf1) -> p(PFM:"Gsk3 Family",pmod(P,S,9))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16086373

4
value: Western blot analyses with epidermal lysates showed that signaling components downstream of PI3K/Akt were altered in epidermis of BK5.IGF-1 mice. Increased phosphorylation of GSK-3 (Ser(9/21)), TSC2(Thr(1462)), and mTOR(Ser(2448)) was observed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16086373

Selventa

RA9rOEIWTQ-32WQ8xY344rlL0y4uI4bmLUfB pOfYZnw8
has assertion: kin(p(HGNC:MAP2K1)) -> kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.302+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP2K1)) -> kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16086581

6
value: Furthermore, we have found that constitutively activated MEK activates JNK. We have corroborated these findings in studies with isolated protein components from a human astrocyte (U-251) cell line; that is, JNK phosphorylates raf but not the reverse; MEK phosphorylates JNK but not the reverse.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16086581

Selventa

RA5uN9hHJi5izqBd52WW1sSexo8IxKfZYxAVVLfgJDQsg
has assertion: a(SCHEM:"Very Low Density Lipoprotein") -> r(HGNC:IL1B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.305+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Very Low Density Lipoprotein") -> r(HGNC:IL1B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087165

3
value: # GeneRif: VLDL induces IL-1beta mRNA expression, caspase-1 activation, and IL-1beta release from macrophages
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087165

Selventa

RAxFs47ykItkLUQLIeFGYthmcqK5UFlN vpDmCIe2tGBQ
has assertion: complex(p(HGNC:ESR1),g(HGNC:B3GNT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.325+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:B3GNT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA9mQU6us3MSykFD0m06voWJjYymmjUNhPcm1jijyXqxE
has assertion: complex(p(HGNC:ESR1),g(HGNC:CTNNBIP1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.330+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:CTNNBIP1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA6osUm5cKTYk423w8goy2NdS5njfRv0CWvALkrt5Guh0
has assertion: complex(p(HGNC:ESR1),g(HGNC:CYP4F3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.332+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:CYP4F3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA mUYppJtatqZQAgIWFXGFIGRSfpHl3o3nP0D5NhgNc
has assertion: complex(p(HGNC:ESR1),g(HGNC:ESR1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.336+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:ESR1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA1PZY4PH3R8uvjdFU965FhOykpRJRGaE4ASEd-LH-XCQ
has assertion: complex(p(HGNC:ESR1),g(HGNC:HSPH1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.338+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:HSPH1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA3C1LBzGM8sOGZtINmsWpNo rblSVWvQH-rgl0cH7MEE
has assertion: complex(p(HGNC:ESR1),g(HGNC:IKBKG))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.340+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:IKBKG))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA9BMNr292tneM9gZiMIwoKE82G8UYrqQjS4myRHbkrFc
has assertion: complex(p(HGNC:ESR1),g(HGNC:IL20))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.341+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:IL20))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAx1l-rFjKcl3RY 8hGsS5xf9Qr7atMqsCZ-ACGJlWGHY
has assertion: complex(p(HGNC:ESR1),g(HGNC:KRT13))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.342+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:KRT13))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA16ZbJnzMC iRwKGw-jooZqR9Ke-AsG8IzNq6nrk56OM
has assertion: complex(p(HGNC:ESR1),g(HGNC:MOCS2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.344+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:MOCS2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA4Hfj9f7KrbetlDyQy566d0ruO5Wh7OTPmdayDxzAcAA
has assertion: complex(p(HGNC:ESR1),g(HGNC:MOCS2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.345+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:MOCS2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAywDhXfFviNnR-9-gxxGk6q sdz Co-0zt7nbfXzM4g8
has assertion: complex(p(HGNC:ESR1),g(HGNC:NR0B2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.350+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:NR0B2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA1k-r9fIDqa5Qp RyRPW4Xz70NN82C --zd86GkhzsTY
has assertion: complex(p(HGNC:ESR1),g(HGNC:PGLYRP2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.355+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:PGLYRP2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAx-NEju625c kl8xlQXRAdOaSqqNpHNevp2JncxYsAmM
has assertion: complex(p(HGNC:ESR1),g(HGNC:PKIB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.356+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:PKIB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA82W8q4 hfAw5bictJN- cSQZb9V7wHO2DRgsjbPtU7U
has assertion: complex(p(HGNC:ESR1),g(HGNC:SLC7A3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.367+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:SLC7A3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA1W76gUE9mUleUGB1dQf0QBVQjq-Co3EEFMJYTKYt8ak
has assertion: complex(p(HGNC:ESR1),g(HGNC:SMYD3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.370+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:SMYD3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER alpha in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA-2IPYBOmQ3pqLUt3bblR8-22KLRRb87CFIBHZ7DYGaA
has assertion: complex(p(HGNC:ESR1),g(HGNC:BANP))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.392+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:BANP))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA7PEl9bLaYf933fzZjzywsCfzYLyzcyHXn0fQ-AqkOSk
has assertion: complex(p(HGNC:ESR1),g(HGNC:CCDC132))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.393+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:CCDC132))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAwuw4wMqMdZuEJLTSY0YGnAF A-rbYBsumXOFX fIgGM
has assertion: complex(p(HGNC:ESR1),g(HGNC:CYP4F3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.397+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:CYP4F3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA4NURAF-RCkxixutAHTcivmgXC3WeMtGTA8OuDA5h1xM
has assertion: complex(p(HGNC:ESR1),g(HGNC:KRT13))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.409+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:KRT13))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAxgk 4myVr2ZClvffWLBk9W wwlkg3GGimI4G1jJTCdU
has assertion: complex(p(HGNC:ESR1),g(HGNC:NINJ2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.415+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:NINJ2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA-f6NswrvXWSEGSm3fzFZXLdflEng7QJnG7-wx4YG8yU
has assertion: complex(p(HGNC:ESR1),g(HGNC:NR0B2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.416+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:NR0B2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA7b1 UD QcbrinixQKbSCmARyD1x6DoxJx-fm722b7yk
has assertion: complex(p(HGNC:ESR1),g(HGNC:PGLYRP2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.422+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:PGLYRP2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA3dkUAUE4toqGnm6bzCgIjChcgk3ZHPecM59HmsL75Ro
has assertion: complex(p(HGNC:ESR1),g(HGNC:PKIB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.423+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:PKIB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RAzftuSQdVB0JqsYfhf3U61KGG9Dv2KhB5Wb4enDnxzeA
has assertion: complex(p(HGNC:ESR1),g(HGNC:RAB7L1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.428+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:RAB7L1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA Hy15dFQh5Wr3yhkPfpapNXmC9nb5U3RYcjbN9QpReo
has assertion: complex(p(HGNC:ESR1),g(HGNC:RBL2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.429+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:RBL2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA6WGM0EjgPOTcIUt2AKLzSCB7vfnjFZhhso-bUMnWUaY
has assertion: complex(p(HGNC:ESR1),g(HGNC:RECQL4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.430+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:RECQL4))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA8bEYAm6KwE5MPwF1q0IESaIyQXZsAG6U5VNaEIHu 8o
has assertion: complex(p(HGNC:ESR1),g(HGNC:SEL1L))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.432+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:SEL1L))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA7zBAzFPll1I05EiFyNor1nRAEmt7PTHR9qjJx5HCK3E
has assertion: complex(p(HGNC:ESR1),g(HGNC:SLC7A3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.434+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:SLC7A3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA9QozbADGUSfu10or4Z 8BWa bqum5eLH0R3iuxHBAfQ
has assertion: complex(p(HGNC:ESR1),g(HGNC:TRIM16))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.444+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ESR1),g(HGNC:TRIM16))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16087863

3
value: Table 1. Functional classification of target genes bound by ER{alpha} in MCF-7 cells in the presence of estradiol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16087863

Selventa

RA1JE76w 7VaIeAFkiKBQT6K8Djno6jaX-uRPPwauW5dM
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:ALOX5AP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.450+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:ALOX5AP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA4OT6RcnCH6F68f6v-H5FlFH0tJy l6d-OB0Dwkkq0mo
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CCL2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.454+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CCL2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA1SXgtGZkepAX1lLB-hTKmxpdIX5gd0FtPDCX9Rk3owU
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CD74)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.459+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CD74)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA6xTA9BHqZfuwfPEFyqTOqDKiTgU0nZkYes5PtgKMIQU
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CXCL2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.462+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CXCL2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA-3op8RVgOihBlK0RCNwinAdsqIsQNRPgYGPwE1bWgro
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CXCR4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.463+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:CXCR4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA8TA6mSOIe0S0Yq5xN LBV93Is4GSn8CphgXNNaPtm8w
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:"HLA-DPA1")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.472+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:"HLA-DPA1")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA9Fd4UXV7KbjqRi4zUM478bSDnS75qJzrVTIKFUV9PSg
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:LYST)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.476+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:LYST)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA-zzY2h FoaiwowS08zmfMo4bLsu 1pl4ut1gu7ag21s
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(HGNC:SELE)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.482+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(HGNC:SELE)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091493

3
value: TABLE 2. Immune response regulated by obesity [obesity vs. lean microarray]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091493

Selventa

RA7U6Fu4hlrNEaX0mH4 qKPvFY-svowg v63EOSRWNvnA
has assertion: p(HGNC:DIABLO) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.485+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:DIABLO) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16091752

3
value: Here, we report that Smac inhibits clonogenic tumor growth by blocking random migration and proliferation and by enhancing apoptosis in a cell density and cell type dependent manner in SH-EP neuroblastoma cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16091752

Selventa

RAxSJla-OUWD9yF-r6-uY6cKFWRftvcqP2tMupeffh-Zg
has assertion: bp(GO:aging) -> r(RGD:Lep)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.489+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(RGD:Lep)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16092054

3
value: The age-related increase of lep gene expression could be, in part, responsible for these changes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16092054

Selventa

RA97QQPYBjXU97Xrabsx38W1Qoj1jLYONpo-OZgp6iBks
has assertion: p(HGNC:CLIP1) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.496+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CLIP1) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16092758

3
value: Restin, a member of melanoma-associated antigen superfamily gene, was first cloned from differentiated leukemia cell induced by all trans-retinoic acid, and was able to inhibit cell proliferation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16092758

Selventa

RA IU6H4vqVm7xmHJsNkngn8-eEdatv8kFwVJXiicWwbk
has assertion: tscript(p(HGNC:ATF3)) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.498+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ATF3)) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16092758

4
value: The results showed that only ATF3 had a strong interaction with Restin. It is interesting to know that ATF3 was an important transcription factor for G1 cell cycle initiation in physiological stress response. It was possible that the inhibition of cell proliferation by Restin might be related with the inhibition of ATF3 activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16092758

Selventa

RA-5X80l1sXPmT TrqAOJ21hqO1GFmTpH3SvVTQY7zqYM
has assertion: a(SCHEM:Hydrocortisone) -| bp(GO:angiogenesis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.502+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Hydrocortisone) -| bp(GO:angiogenesis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093320

2
value: Endogenous glucocorticoids, including those generated locally by 11betaHSD1, exert tonic inhibition of angiogenesis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093320

Selventa

RA0SOryzoVRC43ERBMpNn5xJRHH7MjEHhhY1c0me22uD4
has assertion: complex(p(HGNC:MYCN),g(HGNC:CDK3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.514+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:MYCN),g(HGNC:CDK3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093321

3
value: treatment of LAN-1 cells with 5-aza-C reactivates the expression of CASP8 mRNA (Fig. 6E) and allows the binding of N-Myc to E-box sites (Fig. 6F)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093321

Selventa

RAwmoPh-UokTD1fDTxt5NHLPQbVCfABYbvzLdFpgDfr58
has assertion: complex(p(HGNC:MYCN),g(HGNC:FGFRL1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.516+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:MYCN),g(HGNC:FGFRL1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093321

3
value: treatment of LAN-1 cells with 5-aza-C reactivates the expression of CASP8 mRNA (Fig. 6E) and allows the binding of N-Myc to E-box sites (Fig. 6F)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093321

Selventa

RA oPBodxR0Vo3FB5F-0wHILKAa5rMbJNylD5xqLKLlrY
has assertion: complex(p(HGNC:MYCN),g(HGNC:MEF2A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.523+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:MYCN),g(HGNC:MEF2A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093321

3
value: treatment of LAN-1 cells with 5-aza-C reactivates the expression of CASP8 mRNA (Fig. 6E) and allows the binding of N-Myc to E-box sites (Fig. 6F)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093321

Selventa

RA7eX50V1IxnXZXFYe-X5JvH800hmfdNFFvcerwMTfrB4
has assertion: complex(p(HGNC:MYCN),g(HGNC:PTPRT))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.533+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:MYCN),g(HGNC:PTPRT))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093321

3
value: treatment of LAN-1 cells with 5-aza-C reactivates the expression of CASP8 mRNA (Fig. 6E) and allows the binding of N-Myc to E-box sites (Fig. 6F)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093321

Selventa

RA3H4BMCUE4REmzgrWgV7lbE4sHdVw5Ffm2aLFyYgVE U
has assertion: complex(p(HGNC:MYCN),g(HGNC:TJP1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.539+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:MYCN),g(HGNC:TJP1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16093321

3
value: treatment of LAN-1 cells with 5-aza-C reactivates the expression of CASP8 mRNA (Fig. 6E) and allows the binding of N-Myc to E-box sites (Fig. 6F)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16093321

Selventa

RA g5nvS50M-ffWb39 GbQCzY7sgqAP4Ti0wYviYsM0XY
has assertion: cat(p(HGNC:CMKLR1)) -> bp(GO:"macrophage activation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.551+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:CMKLR1)) -> bp(GO:"macrophage activation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16096270

4
value: direct CMKLR1-positive plasmacytoid dendritic cell and tissue macrophage recruitment to sterile sites of tissue damage, as well as trafficking to sites of infectious and allergic inflammation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16096270

Selventa

RA2OxfU-e1e81iVIWNwkYFQ7xnTgrmCQvCDnV-KGl85E8
has assertion: p(HGNC:LOXL2) -> (tscript(p(HGNC:SNAI1)) -| p(PFH:"CDH Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.553+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:LOXL2) -> (tscript(p(HGNC:SNAI1)) -| p(PFH:"CDH Family"))
label: tscript(p(HGNC:SNAI1)) -| p(PFH:"CDH Family")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16096638

7
value: Here we show that lysyl-oxidase-like 2 and 3 (LOXL2 and LOXL3), two members of the lysyl-oxidase gene family, interact and cooperate with Snail to downregulate E-cadherin expression. Snail's lysine residues 98 and 137 are essential for Snail stability, functional cooperation with LOXL2/3 and induction of EMT
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16096638

Selventa

RA6pX7gV2sT0HsIHh6CsJ0-S EBlotjczzvgN7t1OXa60
has assertion: p(HGNC:SERTAD2) -> tscript(p(HGNC:TP53))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.560+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SERTAD2) -> tscript(p(HGNC:TP53))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16098148

5
value: Expression of SEI-1, SEI-2 or SEI-3 strongly stimulates p53-dependent gene activation in HeLa and U2OS cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16098148

Selventa

RAy50CoyZxtEeTjczNPacbCHTRDvGiRwGQVtSjNv0E8i0
has assertion: tscript(p(MGI:Foxa2)) => r(MGI:Pck1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.611+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) => r(MGI:Pck1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16098831

5
value: Foxa2 occupied its binding sites in all three target genes... Therefore, the decreased activation of the PEPCK, TAT, and IGFBP-1 genes in Foxa2-deficient hepatocytes that we observed solely in the fasted state (Figure 2) indicates that Foxa2 is essential to the transcriptional response to food deprivation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16098831

Selventa

RA8NqdWuJuDX2wLVX3eUh EoMZyRQ3kWQSM8KvnD6 6gM
has assertion: p(HGNC:CTNNB1,pmod(P,Y,654)) => tscript(p(HGNC:CTNNB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.616+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CTNNB1,pmod(P,Y,654)) => tscript(p(HGNC:CTNNB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16099633

5
value: (from text) The phosphorylation of tyrosine 654 increases the ability of ?-catenin to bind the basal transcription factor TATA-binding protein, and mutation of Y654 to glutamate results in enhanced transcriptional activity [33]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16099633

Selventa

RAzrmUWCJOHYfzW4coFxI7-zIZswVZ7I0Et5MSkTEzIPs
has assertion: kin(p(HGNC:EGFR)) => p(HGNC:CTNNB1,pmod(P,Y,654))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.618+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) => p(HGNC:CTNNB1,pmod(P,Y,654))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16099633

5
value: The binding of beta-catenin to these partners is regulated by phosphorylation of at least three critical tyrosine residues. Each of these residues is targeted by one or more specific kinases: Y142 by Fyn, Fer and cMet; Y489 by Abl; and Y654 by Src and the epidermal growth factor receptor.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16099633

Selventa

RA0rqHL5WoYmJ-P iiicmM5QZjfTK9tz313SpIGbHR91o
has assertion: p(HGNC:WWTR1) -| tscript(p(HGNC:PPARG))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.620+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:WWTR1) -| tscript(p(HGNC:PPARG))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16099986

5
value: Here we report that a 14-3-3-binding protein, TAZ (transcriptional coactivator with PDZ-binding motif), coactivates Runx2-dependent gene transcription while repressing PPARgamma-dependent gene transcription.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16099986

Selventa

RA5P68dXsv55R7pYtiJmLU5oY7VrZsvxw1jVP0hibmUkM
has assertion: kin(p(PFH:"PRKC Family")) -> r(HGNC:EGR1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.633+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKC Family")) -> r(HGNC:EGR1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16103054

5
value: HGF-induced expression of Egr-1, PDGFA, and VEGF was suppressed by pharmacologic and siRNA inhibitors of mitogen-activated protein kinase kinase 1/2 (MEK1/2) and protein kinase C (PKC) pathways.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16103054

Selventa

RA4Pt0RJr3GIxcdVh2Rg9ZN0KiVVbgmM7i4bOAr3Z589s
has assertion: tscript(p(MGI:Onecut2)) -> r(MGI:Fst)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.648+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Onecut2)) -> r(MGI:Fst)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16103213

5
value: KO of onecut-2 decreases expression of a2m and follistatin in day 12.5 embryos.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16103213

Selventa

RAzOqRGb5w-TXKPANQoV0ebRLMoKU4AgTcdMPFGvPcyok
has assertion: path(MESHD:Sepsis) -| p(RGD:Cox6a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.654+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Sepsis) -| p(RGD:Cox6a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16103521

3
value: found that sepsis evoked 1) a downregulation of genes encoding all examined electron transport chain components
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16103521

Selventa

RA5Hxa26Us7ZHf-84 ujo28ZXcuhHGX0WN9y7Sj1qNVfk
has assertion: path(MESHD:Sepsis) -| r(RGD:"Atp5h-ps1")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.656+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Sepsis) -| r(RGD:"Atp5h-ps1")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16103521

3
value: found that sepsis evoked 1) a downregulation of genes encoding all examined electron transport chain components
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16103521

Selventa

RA-qr0caobmknXCAp3b0oFi6Hq0m3dHXS5VMKp7xPHqAA
has assertion: path(MESHD:Sepsis) -| r(RGD:Cox6a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.660+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Sepsis) -| r(RGD:Cox6a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16103521

3
value: found that sepsis evoked 1) a downregulation of genes encoding all examined electron transport chain components
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16103521

Selventa

RA2wRn0jtgCMauppestvXx2DvHHXx5fkFYGfeWa21Tjpc
has assertion: composite(a(SCHEM:Diosgenin),a(SCHEM:"Ethinyl estradiol")) -| r(RGD:Abcg5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.662+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(SCHEM:Diosgenin),a(SCHEM:"Ethinyl estradiol")) -| r(RGD:Abcg5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16105132

4
value: Hepatic Abcg5 and Abcg8 mRNA expression decreased in ethinyl estradiol and diosgenin-ethinyl estradiol groups compared with the control group and
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16105132

Selventa

RAyOITOmOQRGNLuxdN2koHkFFrrFBo-SStONONAoAL8I4
has assertion: composite(a(SCHEM:Diosgenin),a(SCHEM:"Ethinyl estradiol")) -> r(RGD:Abcc3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.665+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(SCHEM:Diosgenin),a(SCHEM:"Ethinyl estradiol")) -> r(RGD:Abcc3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16105132

4
value: Hepatic Mrp3 mRNA expression was remarkably increased in the D, EE and DE groups in comparison with the control group (531%, 321% and 1160% of control, respectively, P < 0.01). H
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16105132

Selventa

RA4Iflx zsDHdNpxj48hmcgNgd3lu5oNXbtZsfbGLchLI
has assertion: cat(p(MGI:Ednra)) -> a(SCHEM:"8-Isoprostane")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.674+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Ednra)) -> a(SCHEM:"8-Isoprostane")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16107552

4
value: ET(A) receptor antagonist BQ-123. In AhR null mice, BQ-123 significantly reduced elevated plasma 8-isoprostane, a systemic end product of phospholipid oxidation by ROS,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16107552

Selventa

RA2msxmSUanQEObMP06ta9ZmMeZ5mL75jdUT0O4Qbs0XA
has assertion: r(HGNC:PLD2) -> p(HGNC:MYC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.680+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

r(HGNC:PLD2) -> p(HGNC:MYC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16107734

4
value: Stable elevated expression of PLD2 also increased Myc expression and provided a Myc-dependent survival signal in the absence of E2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16107734

Selventa

RAzR3MKPOcAQ5W-QhPnWuqy5OkIIR5Xu9Qo7aebXTuPsc
has assertion: p(HGNC:BARD1) -| (p(HGNC:BRCA1) -> bp(GO:"cell death"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.690+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BARD1) -| (p(HGNC:BRCA1) -> bp(GO:"cell death"))
label: p(HGNC:BRCA1) -> bp(GO:"cell death")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16108063

5
value: This model for reciprocal regulation of nuclear transport by NES masking is unique in the literature, although it is certainly possible that other heterodimers are regulated in a similar fashion. It is not yet known whether BRCA2 is regulated by nuclear-cytoplasmic shuttling. Functional implications of nuclear-cytoplasmic shuttling of BRCA1 and BARD1 Howdoes the nuclear shuttling ofBRCA1andBARD1regulate their function, and when does it occur? These questions are only now starting to be addressed. The only activity of either BRCA1orBARD1that is yet known to be influenced by nuclear import/export is their ability to induce apoptosis when overexpressed; apoptotic activity of both BRCA1(45) and of BARD1(51) is inhibited by at least 50% when the two proteins are co-expressed in cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16108063

Selventa

RA3U4cGnAI7f6ZstA8FCiOsxhZKhBxFEOqlnSapgN 8-0
has assertion: p(HGNC:BRCA1) -> bp(GO:"cell death")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.691+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BRCA1) -> bp(GO:"cell death")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16108063

3
value: This model for reciprocal regulation of nuclear transport by NES masking is unique in the literature, although it is certainly possible that other heterodimers are regulated in a similar fashion. It is not yet known whether BRCA2 is regulated by nuclear-cytoplasmic shuttling. Functional implications of nuclear-cytoplasmic shuttling of BRCA1 and BARD1 Howdoes the nuclear shuttling ofBRCA1andBARD1regulate their function, and when does it occur? These questions are only now starting to be addressed. The only activity of either BRCA1orBARD1that is yet known to be influenced by nuclear import/export is their ability to induce apoptosis when overexpressed; apoptotic activity of both BRCA1(45) and of BARD1(51) is inhibited by at least 50% when the two proteins are co-expressed in cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16108063

Selventa

RA5z6meUamHeTiNBypbxO9BjRpq AzzPvyES9HudPsdYo
has assertion: kin(p(HGNC:MAP2K1)) -> kin(p(HGNC:IKBKB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.695+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP2K1)) -> kin(p(HGNC:IKBKB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16113098

6
value: Endocrine therapy with an estrogen receptor (ER)-targeted antiestrogen, such as tamoxifen, or estrogen ablation by aromatase inhibitors is clinically indicated for the management of all forms of ER-positive breast cancer. However, 30-50% of ER-positive breast cancer cases fail to benefit clinically from endocrine therapy alone, and recent molecular evidence suggests that 'crosstalk' pathways originating from activated receptor tyrosine kinases and/or other proliferative and survival signals may be contributing to this endocrine resistance. Molecular identification and validation of candidate ER crosstalking pathways will likely lead to clinically important prognostic markers and targets for the application of novel therapeutics in combination with standard endocrine agents. This review focuses on a critical survival and proliferation pathway involving activation of nuclear factor-kappaB (NFkappaB), a family of ubiquitously expressed transcription factors that for nearly two decades have been known to be critical regulators of mammalian immune and inflammatory responses, and more recently have been associated with chemotherapy resistance. With the demonstration that activation of NFkappaB is absolutely required for normal mammary gland development, NFkappaB involvment in human breast cancers was initially explored and linked to the development of hormone-independent (ER-negative) breast cancer. Newer clinical evidence now implicates NFkappaB activation, particularly DNA-binding by the p50 subunit of NFkappaB, as a potential prognostic marker capable of identifying a high-risk subset of ER-positive, primary breast cancers destined for early relapse despite adjuvant endocrine therapy with tamoxifen. Furthermore, initial preclinical studies suggest that treatment strategies designed to prevent or interrupt activation of NFkappaB in cell-line models of these more aggressive, ER-positive breast cancers can restore their sensitivity to such standard endocrine agents as tam[cell cut: 2007 characters, first 2000 kept]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16113098

Selventa

RA6PlzI55bzjMjydeBjuI2645I42hV8rTouXFZaOIEmgs
has assertion: p(HGNC:AKT1,pmod(P,S)) => kin(p(HGNC:AKT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.698+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AKT1,pmod(P,S)) => kin(p(HGNC:AKT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16114056

5
value: CXCR4 was localized to lipid rafts in PC cells and initiated Akt phosphorylation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16114056

Selventa

RA9w7Usir9XhtdypqL-Poys24PuQvEtqSnxCdy0-hR-tA
has assertion: p(HGNC:RALBP1) -> (p(HGNC:TNF) -> kin(p(HGNC:IKBKB)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.707+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:RALBP1) -> (p(HGNC:TNF) -> kin(p(HGNC:IKBKB)))
label: p(HGNC:TNF) -> kin(p(HGNC:IKBKB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16115877

7
value: Rip1 is required for IkappaB kinase activation in response to tumor necrosis factor alpha (TNF-alpha) and has been implicated in the Toll-like receptor 3 (TLR3) response to double-stranded RNA.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16115877

Selventa

RAzYx-FcHpdXKo2rIOf3su9f0doWRYs8H5G1cre0frouw
has assertion: cat(p(HGNC:TLR3)) => complex(p(HGNC:TLR3),p(HGNC:MAP3K7))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.710+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:TLR3)) => complex(p(HGNC:TLR3),p(HGNC:MAP3K7))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16115877

7
value: Upon TLR3 activation, Rip1 is also modified by polyubiquitin chains and is recruited to TLR3 along with Traf6 and the ubiquitin-activated kinase Tak1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16115877

Selventa

RA3KeyP12JOdVGbB2kzDliD0tYlLDXEcY LeCvjAb0Ox4
has assertion: p(HGNC:PTN) -> kin(p(HGNC:PRKCA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.716+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PTN) -> kin(p(HGNC:PRKCA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16116087

5
value: We now demonstrate that PTN stimulates the phosphorylation of serines 713 and 726 in the myristoylated alanine-rich protein kinase (PK) C substrate domain of beta-adducin through activation of either PKC alpha or beta.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16116087

Selventa

RAyfDbR5Onr1uVAqCB9uL0Dog WF7ek5HhppxUGyQ10aA
has assertion: tscript(p(HGNC:FOXO4)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.722+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:FOXO4)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16116430

4
value: By using viral-mediated MEOX2 gene silencing and transfer, we show that restoring expression of the protein it encodes, GAX, in BECs from individuals with Alzheimer disease stimulates angiogenesis, transcriptionally suppresses AFX1 forkhead transcription factor-mediated apoptosis and increases the levels of a major amyloid-beta peptide (Abeta) clearance receptor, the low-density lipoprotein receptor-related protein 1 (LRP), at the blood-brain barrier
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16116430

Selventa

RA2y P0n0QYUR28NIuHXHu9KWPfFbIfuSBOSJNpYML0U8
has assertion: tscript(p(HGNC:FOXO4)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.726+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:FOXO4)) -> bp(MESHPP:Apoptosis)
label: tscript(p(HGNC:MEOX2)) -| (tscript(p(HGNC:FOXO4)) -> bp(MESHPP:Apoptosis))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16116430

7
value: By using viral-mediated MEOX2 gene silencing and transfer, we show that restoring expression of the protein it encodes, GAX, in BECs from individuals with Alzheimer disease stimulates angiogenesis, transcriptionally suppresses AFX1 forkhead transcription factor-mediated apoptosis and increases the levels of a major amyloid-beta peptide (Abeta) clearance receptor, the low-density lipoprotein receptor-related protein 1 (LRP), at the blood-brain barrier
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16116430

Selventa

RAzPbqbaJzxPRkqt7vePgUDSnSV56lLJMYZ7FZaMlUiFc
has assertion: cat(p(HGNC:SCD)) -> a(CHEBI:lipid)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.730+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SCD)) -> a(CHEBI:lipid)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16118274

4
value: Stearoyl-CoA desaturase-2 gene expression is required for lipid synthesis during early skin and liver development.\" There are four known stearoyl-CoA desaturase (SCD) enzyme isoforms in mouse and two in humans that are required for the biosynthesis of monounsaturated fatty acids, mainly oleate.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16118274

Selventa

RA9ikmL5Ql ap6If7jW-SDjxe4qrsiPnK7xgkbnV6E Aw
has assertion: a(CHEBI:calcitriol) -| r(MGI:Cxcl10)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.731+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -| r(MGI:Cxcl10)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16118315

3
value: Among these are the suppression of listericidal activity, the inhibition of phagocyte oxidase-mediated oxidative burst, and the suppression of important IFN-gamma-induced genes, including Ccl5, Cxcl10, Cxcl9, Irf2, Fcgr1, Fcgr3, and Tlr2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16118315

Selventa

RA-FXYoT8v3lNKcF ZGgfIqYazGl7mzWKjeboBYpkkZiA
has assertion: a(CHEBI:calcitriol) -| r(MGI:Fcgr1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.734+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -| r(MGI:Fcgr1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16118315

3
value: Among these are the suppression of listericidal activity, the inhibition of phagocyte oxidase-mediated oxidative burst, and the suppression of important IFN-gamma-induced genes, including Ccl5, Cxcl10, Cxcl9, Irf2, Fcgr1, Fcgr3, and Tlr2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16118315

Selventa

RA4NUeCwxacQo5AA3FKWdZbDUK4WKJXLlAieHMH4z94iw
has assertion: a(CHEBI:calcitriol) -| r(MGI:Irf2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.736+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -| r(MGI:Irf2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16118315

3
value: Among these are the suppression of listericidal activity, the inhibition of phagocyte oxidase-mediated oxidative burst, and the suppression of important IFN-gamma-induced genes, including Ccl5, Cxcl10, Cxcl9, Irf2, Fcgr1, Fcgr3, and Tlr2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16118315

Selventa

RA2RZ4ze5EFBhW3NCXgqor ROVEodCpTfctTppHk6KvUE
has assertion: a(CHEBI:calcitriol) -| r(MGI:Tlr2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.737+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:calcitriol) -| r(MGI:Tlr2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16118315

3
value: Among these are the suppression of listericidal activity, the inhibition of phagocyte oxidase-mediated oxidative burst, and the suppression of important IFN-gamma-induced genes, including Ccl5, Cxcl10, Cxcl9, Irf2, Fcgr1, Fcgr3, and Tlr2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16118315

Selventa

RA1faZnGAOJP8CvVaGSj18Vs2464kDIC7naIgXVSHthmo
has assertion: tscript(p(MGI:Atf4)) -| tscript(p(MGI:Creb1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.747+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Atf4)) -| tscript(p(MGI:Creb1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16121183

6
value: in the hippocampus of GCN2(-/-) mice, the expression of ATF4 is reduced and CREB activity is increased
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16121183

Selventa

RA ApoEbvZQrTewdjb7fLljT4Ptsz7Gc3I5QCF8mbRHHg
has assertion: bp(GO:"response to UV") -> p(MGI:Egfr,pmod(P,Y,1173))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.748+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV") -> p(MGI:Egfr,pmod(P,Y,1173))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16123117

3
value: EGFR was rapidly activated in mouse epidermis following exposure to UV, as detected by the phosphorylation of EGFR on tyrosine residues 992, 1045, 1068 and 1173.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16123117

Selventa

RA7QS-41ih0XpqaNxN71hbDsGQ8qdPmZUFUQkkU137N3I
has assertion: kin(p(PFH:"AKT Family")) -> p(HGNC:RNF11,pmod(P,T,135))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.754+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"AKT Family")) -> p(HGNC:RNF11,pmod(P,T,135))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16123141

5
value: RNF11 is phosphorylated by AKT in vitro and is recognized by phospho-AKT substrate antibodies.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16123141

Selventa

RA2inmwwdgstsXPz67wSK10m-lIfSzQ9O oojCLDdVKqo
has assertion: p(MGI:Pdx1) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.757+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Pdx1) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16123346

3
value: Pdx1 repression was associated with increased cell proliferation predominantly in the exocrine pancreas and upregulation of genes implicated in pancreas regeneration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16123346

Selventa

RA K28h4NSoAk1ZQEhmHV1H8sfT2hbX1qO5srg-qKNybI
has assertion: p(MGI:Sox6) -| r(MGI:Atp2a2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.758+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox6) -| r(MGI:Atp2a2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16124007

4
value: We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16124007

Selventa

RA30KAtAEn6O1FhNXt4bcZAiFseqWGw334SxlFjduVSDA
has assertion: p(MGI:Sox6) -| r(MGI:Myl4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.762+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox6) -| r(MGI:Myl4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16124007

4
value: We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16124007

Selventa

RAzDD1bcfNqtAD0oAncBNF7iWq04aUVHMAlay3P3WVMJU
has assertion: p(MGI:Sox6) -| r(MGI:Myh7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.765+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox6) -| r(MGI:Myh7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16124007

4
value: We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16124007

Selventa

RA8UaLN-eD2eHcfsHOtUOzijiewHv8DEw7NgLEHiGqh-A
has assertion: p(MGI:Sox6) -| r(MGI:Tnnt2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.767+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox6) -| r(MGI:Tnnt2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16124007

4
value: We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16124007

Selventa

RA9TLLHgRy4JbQAbeVqtyCx xK4ieyCJIek1tlueV97Z0
has assertion: p(MGI:Sox6) -> r(MGI:Pvalb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.775+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Sox6) -> r(MGI:Pvalb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16124007

4
value: We have previously demonstrated that p100H mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p100H mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p100H mutant, the present results suggest that Sox6 likely plays an important role in muscle development.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16124007

Selventa

RAy5xElDym6dBmGiSJg1X3RmdkA3zxqVMiAroHIBn4eWE
has assertion: a(SCHEM:"Dietary Lipid") -| r(MGI:Cfh)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.786+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -| r(MGI:Cfh)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA e1aBl8hkA3NfyPLhS8gzO6sNc2keiWkwMRRyK7q-k
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.793+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA8y91RyiYXBc2NWcU0yKhcg-gNZbMULhwuRzpdrJ yE0
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.798+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA7N9S3stBUa1peN4Rsd83c6e6rBEle7WNX14FGdV1cig
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Cd83)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.807+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Cd83)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RAxpMhOGdZX5RzbX80lTLQsBwbDyx3T8B-uzxiAFrKPAg
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Cd84)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.808+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Cd84)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RAzpyviORJ2IW3WgVos-V-IacOuqBj2HTe5dpPBArgxZA
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Cd93)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.810+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Cd93)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA0k11OjS81Ucwxnihvn4QJVgzMkGs905lzohJQLcaWnA
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl9)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.816+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Ccl9)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RAysqqjIZpeO5PqK3NuVm6l09abrn2UUei KbhBZb53Rc
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Il2rg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.826+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Il2rg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA ZlXM7CpE185sZdelft8UfEdxXwtMViGF0FgrVmdSWY
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Il6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.829+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Il6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA0lSb7vtEmHGkFwbKuZcxidAfwOaRV95trUrIkUDAmsY
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Il7r)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.835+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Il7r)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA2JH0gCHGhIvtV3osEh3nSGV9noRkWUjqc65emm1NgkA
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Msr1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.840+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Msr1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA9jJJeFIuWb28k--7SBXdeAdScR8qFlsRlpLYbx65AIo
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Ncf4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.842+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Ncf4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA60MF9dI5h GXseoRQpwKE2azDhc4GcnIk8ZkLVNiPG4
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Tlr6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.850+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Tlr6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA8BslmbpKh3xOT1LjbG4R6rBOSL2aP6610MWYCNjDrgo
has assertion: a(SCHEM:"Dietary Lipid") -> r(MGI:Traf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.854+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Dietary Lipid") -> r(MGI:Traf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16129712

3
value: OBJECTIVE: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and -3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue. RESEARCH METHODS AND PROCEDURES: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody. RESULTS: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-alpha. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2. DISCUSSION: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16129712

Selventa

RA29qVYSlCtIXFKhfXJ1Ay1M36JkpGYv2Q9f2QDDdh7oo
has assertion: complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> p(HGNC:ACTB,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.862+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> p(HGNC:ACTB,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135530

6
value: Mass spectral identification of radiolabeled c-Src-as1 substrates revealed several direct targets of c-Src upon PDGF stimulation: PDGFR (from one-dimensional gel), vimentin, tubulin-{beta}5, {beta}- and {gamma}-actin, and myosin light chain 2-A
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135530

Selventa

RA BAJArtRLUAwWP5ZlFQ2Ke9edOafM5cFCS9gMxASNN8
has assertion: complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> p(HGNC:MYL7,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.865+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> p(HGNC:MYL7,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135530

6
value: Mass spectral identification of radiolabeled c-Src-as1 substrates revealed several direct targets of c-Src upon PDGF stimulation: PDGFR (from one-dimensional gel), vimentin, tubulin-{beta}5, {beta}- and {gamma}-actin, and myosin light chain 2-A
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135530

Selventa

RA4YkYKYaQE7-YEe7o6Q9KoZhHS4hdfWhCCOTJ65TQ4Q0
has assertion: complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> bp(GO:chemotaxis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.868+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> bp(GO:chemotaxis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135530

5
value: PDGF-dependent chemotaxis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135530

Selventa

RA QDFjU9ms-N0RDzUDdOtKtdGx7ZQB AfLWHXDVomhiE
has assertion: complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> kin(p(HGNC:FYN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.884+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PDGFB),p(HGNC:PDGFB)) -> kin(p(HGNC:FYN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135530

7
value: exposure to PDGF resulted in a marked increase in c-Src, Fyn, and Yes kinase activities
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135530

Selventa

RA6li pTjLGFo0W0Uy93LgNx9FG0yVfzjz7QXwC7hEFBY
has assertion: kin(p(HGNC:SRC)) -> bp(GO:chemotaxis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.889+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:SRC)) -> bp(GO:chemotaxis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135530

4
value: the observed 70% decrease in chemotactic response can be solely attributed to c-Src inhibition.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135530

Selventa

RA89pAMxdSULZoKKv1SuqvDbWOoIDwUzruI-L2mh2U7Os
has assertion: p(HGNC:SMARCE1) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SMARCE1) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135788

3
value: Altered growth was found to be due in part to cell cycle arrest and induction of apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135788

Selventa

RA4GvvvkF8G4kNuLgxkkljNHndCTmgNAURKxULoR iuZQ
has assertion: p(HGNC:CYLD) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.894+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CYLD) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135788

3
value: Increased expression of CYLD in BT549 cells induced apoptosis, while its suppression by small interfering RNA inhibited cell death in BAF57 expressing BT549 cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135788

Selventa

RAydpLfZYmR mLtIVKxnMlwDcx5iOdxBY8YGrK8 qDqAo
has assertion: p(MGI:Rela,pmod(A,K,310)) => tscript(p(MGI:Rela))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.898+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Rela,pmod(A,K,310)) => tscript(p(MGI:Rela))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135789

5
value: These findings indicate that the acetylation of RelA at lysine 310 is importantly regulated by prior phosphorylation of serines 276 and 536. Such phosphorylated and acetylated forms of RelA display enhanced transcriptional activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135789

Selventa

RA3J4sURPgJB5-0ArRq-k8meutII4xaolHMGWi4sy4i4A
has assertion: p(HGNC:TGFB1) -> complex(p(HGNC:SMAD2),p(HGNC:SMAD3),p(HGNC:SMAD4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.908+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFB1) -> complex(p(HGNC:SMAD2),p(HGNC:SMAD3),p(HGNC:SMAD4))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16135802

7
value: In response to transforming growth factor beta (TGF-beta), Smad4 forms complexes with activated Smad2 and Smad3, which accumulate in the nucleus,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16135802

Selventa

RA0sYjIwQDdYAT4ChUzpRWA5eVEfFC0POBvKJZkFkeJdY
has assertion: kin(p(HGNC:CHEK1)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.913+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:CHEK1)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16137618

4
value: The ubiquitination of Chk1 is mediated by E3 ligase complexes containing Cul1 or Cul4A. Treatment of cells with the anticancer agent camptothecin (CPT) triggers Chk1 destruction, which blocks recovery from drug-induced S phase arrest and leads to cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16137618

Selventa

RA12xJzSPJ1lBmXF3 FNP6-TWxPDH4c1HKFm8hiUICbo
has assertion: cat(p(HGNC:CNR2)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.916+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:CNR2)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16139274

4
value: Results show that stimulation of the CB2 receptor leads to p38 MAPK activation and that inhibition of this kinase attenuates CB2 receptor-induced caspase activation and apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16139274

Selventa

RA7rt8iKaoyDNERiwgLWGGIJWW3o3flb-nZyVHtuEU5N0
has assertion: p(HGNC:PARP1) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.920+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PARP1) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16140981

3
value: Collectively, these studies suggest that the persistent single-strand breaks formed upon PARP-1 inhibition, which promote the collapse of replication forks and would normally be repaired by homologous recombination, cannot be repaired effectively in the absence of functional BRCA1 or BRCA2. This results in the accumulation of chromosomal abnormalities, cell cycle arrest in G2/M, and apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16140981

Selventa

RAwXPe2pOaxn9fsh5w5pl1VwLyzT2SMlo8rJtR0p6Gyh0
has assertion: cat(p(MGI:Tnfrsf1b)) -> p(MGI:Mapk1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.923+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Tnfrsf1b)) -> p(MGI:Mapk1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141211

5
value: Intestinal fibrosis is an incurable complication of Crohn's disease involving increased numbers of collagen-producing myofibroblasts. Tumor necrosis factor (TNF) alpha has defined proinflammatory roles in Crohn's disease but its role in fibrosis is unclear. We tested the hypothesis that TNFalpha increases collagen accumulation and proliferation in intestinal myofibroblasts and has additive effects in combination with insulin-like growth factor (IGF) I. The mechanisms, TNF receptor isoform, and downstream signaling pathways were examined. Intestinal myofibroblasts from wild-type (WT) mice or mice homozygous for disruption of genes encoding TNFR1 (TNFR1-/-), TNFR2 (TNFR2-/-), or both (TNFR1/2-/-), were treated with TNFalpha, IGF-I, or both. In WT cells, TNFalpha and IGF-I stimulated type I collagen accumulation and DNA synthesis in an additive manner. IGF-I, but not TNFalpha, stimulated type I collagen gene activation. TNFalpha, but not IGF-I, induced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degradation. TNFalpha also activated ERK1/2. These responses to TNFalpha were absent in TNFR2-/- and TNFR1/2-/- myofibroblasts, whereas TNFR1-/- cells showed similar responses to WT. Inhibition of ERK1/2 diminished TNFalpha induced DNA synthesis in WT and TNFR1-/- cells. Differences in TNFalpha-induced STAT3/DNA binding activity and not NFkappaB and AP-1 transcriptional activation correlated with impaired collagen accumulation/TIMP-1 induction in TNFR2(-/-) cells. Constitutively active STAT3 rescued TIMP-1 expression in TNFR2-/- cells. We conclude that TNFalpha and IGF-I may additively contribute to fibrosis during intestinal inflammation. TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141211

Selventa

RAwybhggq8xe0xYyZAPyTzKYeviLVoNVImQMmhVjtRKWg
has assertion: kin(p(PFM:"MAPK Erk1/3 Family")) -> tscript(p(MGI:Stat3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.924+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFM:"MAPK Erk1/3 Family")) -> tscript(p(MGI:Stat3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141211

6
value: Intestinal fibrosis is an incurable complication of Crohn's disease involving increased numbers of collagen-producing myofibroblasts. Tumor necrosis factor (TNF) alpha has defined proinflammatory roles in Crohn's disease but its role in fibrosis is unclear. We tested the hypothesis that TNFalpha increases collagen accumulation and proliferation in intestinal myofibroblasts and has additive effects in combination with insulin-like growth factor (IGF) I. The mechanisms, TNF receptor isoform, and downstream signaling pathways were examined. Intestinal myofibroblasts from wild-type (WT) mice or mice homozygous for disruption of genes encoding TNFR1 (TNFR1-/-), TNFR2 (TNFR2-/-), or both (TNFR1/2-/-), were treated with TNFalpha, IGF-I, or both. In WT cells, TNFalpha and IGF-I stimulated type I collagen accumulation and DNA synthesis in an additive manner. IGF-I, but not TNFalpha, stimulated type I collagen gene activation. TNFalpha, but not IGF-I, induced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degradation. TNFalpha also activated ERK1/2. These responses to TNFalpha were absent in TNFR2-/- and TNFR1/2-/- myofibroblasts, whereas TNFR1-/- cells showed similar responses to WT. Inhibition of ERK1/2 diminished TNFalpha induced DNA synthesis in WT and TNFR1-/- cells. Differences in TNFalpha-induced STAT3/DNA binding activity and not NFkappaB and AP-1 transcriptional activation correlated with impaired collagen accumulation/TIMP-1 induction in TNFR2(-/-) cells. Constitutively active STAT3 rescued TIMP-1 expression in TNFR2-/- cells. We conclude that TNFalpha and IGF-I may additively contribute to fibrosis during intestinal inflammation. TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141211

Selventa

RA1z2LeVNXwI4JN66pUklxZnvO0ze8Wy7oBJmhFgaHBOM
has assertion: bp(GO:"double-strand break repair") -| a(SCHEM:"double-stranded DNA break")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.932+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"double-strand break repair") -| a(SCHEM:"double-stranded DNA break")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141230

2
value: Our findings suggest a role for RECQL4 in the repair of DNA double-strand breaks by homologous recombination and shed new light onto RECQL4's function in human cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141230

Selventa

RA6av-XBI47MtPwwZLz4dhUiIcheM3lTyh4Q0fewHX9uI
has assertion: complex(p(HGNC:RAD51),p(HGNC:RECQL4)) -> bp(GO:"double-strand break repair")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.933+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:RAD51),p(HGNC:RECQL4)) -> bp(GO:"double-strand break repair")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141230

5
value: Our findings suggest a role for RECQL4 in the repair of DNA double-strand breaks by homologous recombination and shed new light onto RECQL4's function in human cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141230

Selventa

RA0XPwG-WwJkNZPW5pdarzi7jgga2c3HRYus0-tcsr7-0
has assertion: p(HGNC:THBS1) -| kin(p(HGNC:MAPK3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.936+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:THBS1) -| kin(p(HGNC:MAPK3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141331

5
value: Both the growth-stimulating activity of low-dose NO for endothelial cells and suppression of TSP1 expression were ERK-dependent. Conversely, exogenous TSP1 suppressed NO-mediated pERK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141331

Selventa

RA6vSM4Z6EGCPDfMctELb5W2wLeP-64gLRgA2dyv8umh8
has assertion: kin(p(HGNC:MAPK1)) -> bp(GO:"cell growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.939+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK1)) -> bp(GO:"cell growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16141331

4
value: Both the growth-stimulating activity of low-dose NO for endothelial cells and suppression of TSP1 expression were ERK-dependent. Conversely, exogenous TSP1 suppressed NO-mediated pERK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16141331

Selventa

RA3aBFK94bG-2BweboEHC478CHdnzarrLHmI8nxTyjc8o
has assertion: p(HGNC:TP53,sub(P,309,S)) =| tscript(p(HGNC:TP53))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.944+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

1
has substitution: P,309,S
variant of: http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11998
type: http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00000

p(HGNC:TP53,sub(P,309,S)) =| tscript(p(HGNC:TP53))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16142585

5
value: From mutations file
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16142585

Selventa

RA0yf1eUREFYF876SAjE9YOXVfYZQqZTIAAtjL TXlHuk
has assertion: cat(p(MGI:Ticam1)) -> tscript(p(MGI:Irf3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.948+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Ticam1)) -> tscript(p(MGI:Irf3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16143103

6
value: TLR3 and TLR4 activate IRF3 and NF-kappaB through the TRIF-dependent pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16143103

Selventa

RA-L qTMHV UyB87Y58QoXETKEtqztt BL1QnRX ek5e0
has assertion: cat(p(MGI:Tlr3)) -> tscript(p(MGI:Irf3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.951+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Tlr3)) -> tscript(p(MGI:Irf3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16143103

6
value: TLR3 and TLR4 activate IRF3 and NF-kappaB through the TRIF-dependent pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16143103

Selventa

RA9h6NXhgTz49yUjebY4bvMW4IAob8l7MdYY0FGL83Y4M
has assertion: p(HGNC:BMP2) -> p(HGNC:SMAD1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.968+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BMP2) -> p(HGNC:SMAD1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16144844

4
value: SMAD1 phosphorylation was examined in C-28/I2 chondrocytes treated with BMP2(100ng/ml). It was phosphorylated after treatment with BMP2 for 1 hour.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16144844

Selventa

RAzcZWlC6fD5a IyiL9yilTVTm8jVif0polTC8j 9AS4
has assertion: a(CHEBI:phenylalanine) -> r(MGI:Col1a2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.977+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:phenylalanine) -> r(MGI:Col1a2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16150627

3
value: Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by phenylalanine hydroxylase (PAH) deficiency. Accumulation of phenylalanine leads to severe mental and psychomotor retardation, and hypopigmentation of skin and hair...Our data indicated that 12 genes were significantly up-regulated in PKU. Four are involved in defense and inflammatory responses of neutrophils (NE, MPO, NGP, and CRAMP), three other overexpressed genes are related to extracellular matrix organization and degradation (COL1A1, COL1A2, and MMP13); the remainder were a nociceptor in sensory neurons (MrgA1), a structural gene of P lysozyme (Lzp-s), an immunoglobulin alpha heavy chain constant region gene (Igh-2), an osteocalcin-related protein precursor (Bglap-rs1), and a membrane-spanning 4 domain, subfamily A, member 3 (Ms4a3).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16150627

Selventa

RA7uRBTL mWhc8aTuHQoxRDl6cEKp9Su14PJGnpRbQzn0
has assertion: a(CHEBI:phenylalanine) -> r(EGID:50701)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.981+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:phenylalanine) -> r(EGID:50701)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16150627

3
value: Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by phenylalanine hydroxylase (PAH) deficiency. Accumulation of phenylalanine leads to severe mental and psychomotor retardation, and hypopigmentation of skin and hair...Our data indicated that 12 genes were significantly up-regulated in PKU. Four are involved in defense and inflammatory responses of neutrophils (NE, MPO, NGP, and CRAMP), three other overexpressed genes are related to extracellular matrix organization and degradation (COL1A1, COL1A2, and MMP13); the remainder were a nociceptor in sensory neurons (MrgA1), a structural gene of P lysozyme (Lzp-s), an immunoglobulin alpha heavy chain constant region gene (Igh-2), an osteocalcin-related protein precursor (Bglap-rs1), and a membrane-spanning 4 domain, subfamily A, member 3 (Ms4a3).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16150627

Selventa

RA42ozJobp4KRDPHoy5QohIqGpTFtzEJf0YogdAl8UpmY
has assertion: a(CHEBI:phenylalanine) -> r(MGI:Lyz1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.983+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:phenylalanine) -> r(MGI:Lyz1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16150627

3
value: Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by phenylalanine hydroxylase (PAH) deficiency. Accumulation of phenylalanine leads to severe mental and psychomotor retardation, and hypopigmentation of skin and hair...Our data indicated that 12 genes were significantly up-regulated in PKU. Four are involved in defense and inflammatory responses of neutrophils (NE, MPO, NGP, and CRAMP), three other overexpressed genes are related to extracellular matrix organization and degradation (COL1A1, COL1A2, and MMP13); the remainder were a nociceptor in sensory neurons (MrgA1), a structural gene of P lysozyme (Lzp-s), an immunoglobulin alpha heavy chain constant region gene (Igh-2), an osteocalcin-related protein precursor (Bglap-rs1), and a membrane-spanning 4 domain, subfamily A, member 3 (Ms4a3).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16150627

Selventa

RA-0a-cOBHlJOXEcrwcKahzX5VtZHa2 f3hdWXC0wzdg0
has assertion: a(CHEBI:"reactive oxygen species") -> p(RGD:Cav1,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:37.995+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"reactive oxygen species") -> p(RGD:Cav1,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16151024

3
value: The nonreceptor tyrosine kinase, proto-oncogene cAbl is a substrate of Src and is a major mediator for ROS-dependent tyrosine phosphorylation of Cav1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16151024

Selventa

RA53lKUOc0v3Wf9p-eu9XEYSYqDFig8d3cOVhJF6cRucc
has assertion: kin(p(PFH:"PRKA Family")) => p(HGNC:PDE3A,pmod(P,S,312))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.000+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) => p(HGNC:PDE3A,pmod(P,S,312))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16153182

5
value: Forskolin did not promote the binding of 14-3-3 proteins to PDE3A (Figures 2A and 5A). However, using the pSer312-PDE3A antibodies, we found that forskolin stimulated the phosphorylation of PDE3A at Ser312 (Figures 5A and 5C). This residue lies within a sequence SHRRTS312LPCIP that conforms to a consensus site for PKA. The forskolin-stimulated phosphorylation of Ser312 was inhibited by the PKA inhibitor H-89 (Figure 5C), and by mimosine and aphidicolin (Figure 5A), but not by inhibitors of PI3K (LY 294002), mTOR (mammalian target of rapamycin) (rapamycin) or the MAPK cascade (U0126) (Figure 5C; see [35] for inhibitor specificities), nor by H-7 (results not shown).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16153182

Selventa

RAysg VKBzwVt2kUxJTLQgv26N3kO0vC1M88wi9edj32c
has assertion: kin(p(PFH:"PRKC Family")) => p(HGNC:PDE3A,pmod(P,S,428))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.001+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKC Family")) => p(HGNC:PDE3A,pmod(P,S,428))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16153182

5
value: PDE3A (phosphodiesterase 3A) was identified as a phosphoprotein that co-immunoprecipitates with endogenous 14-3-3 proteins from HeLa cell extracts, and binds directly to 14-3-3 proteins in a phosphorylation-dependent manner (Ser428). Among cellular stimuli tested, PMA promoted maximal binding of PDE3A to 14-3-3 proteins. While p42/p44 MAPK (mitogen-activated protein kinase), SAPK2 (stress-activated protein kinase 2)/p38 and PKC (protein kinase C) were all activated by PMA in HeLa cells, the PMA-induced binding of PDE3A to 14-3-3 proteins was inhibited by the non-specific PKC inhibitors Ro 318220 and H-7, but not by PD 184352, which inhibits MAPK activation, nor by SB 203580 and BIRB0796, which inhibit SAPK2 activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16153182

Selventa

RA8rPumm8pv09IqxM-0dkAiZ6wap6e7fQwlSQf02b54rc
has assertion: kin(p(HGNC:RET)) => p(HGNC:PTK2,pmod(P,Y,576))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.003+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RET)) => p(HGNC:PTK2,pmod(P,Y,576))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16153436

5
value: RESULTS: Immunoprecipitated, mutant RET from cells or the recombinant RET kinase domain was able to directly phosphorylate tyrosine residues on FAK. Specifically Y576/577, Y861, and Y925, but not the autophosphorylation site Y397 of FAK, were phosphorylated by RET.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16153436

Selventa

RA-PYNqGjRwIBoPWv90luehR7QoIon2repRNnpwbb9WU0
has assertion: a(CHEBI:aldosterone) -> bp(GO:"response to oxidative stress")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.016+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:aldosterone) -> bp(GO:"response to oxidative stress")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16156509

2
value: Aldosterone seems to induce cardiac inflammation and gene expression via oxidative stress that is inhibited by N-acetylcysteine but not by tempol.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16156509

Selventa

RA0OTZpphFvpAkGDXxfhWsQh2JMmq14-ozadN0SXu8ZcY
has assertion: p(MGI:Aifm1) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.019+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Aifm1) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16156740

3
value: Reduction of AIF expression by RNA interference inhibited large-scale DNA fragmentation and conferred significant protection against MPP+ toxicity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16156740

Selventa

RA 1CtAsunR2UDQIErqLSy2BeOr9oqbBkPlUNbfom8Ndg
has assertion: tscript(p(MGI:Sp1)) -> bp(GO:angiogenesis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.030+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Sp1)) -> bp(GO:angiogenesis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16158248

4
value: Furthermore, knocking down Sp1 expression significantly impaired the angiogenic potential of tumor cells in vitro and suppressed angiogenesis in vivo animal models.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16158248

Selventa

RA CCjJLHSou8cTbkaWtgd5Rdv4qj6AHW3TqKifdh7Vgo
has assertion: p(MGI:Retn) -> p(MGI:Vcam1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.033+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Retn) -> p(MGI:Vcam1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16159596

4
value: Incubation of murine aortic ECs with recombinant resistin increased monocyte chemoattractant protein (MCP)-1 and soluble vascular cell adhesion molecule (sVCAM)-1 protein levels in the conditioned medium.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16159596

Selventa

RA5UvM Z2ASc6HRTZRqigNKw idzQBpxIiRsja3I37kZY
has assertion: p(MGI:Retn) -> sec(p(MGI:Ccl2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.034+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Retn) -> sec(p(MGI:Ccl2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16159596

5
value: Incubation of murine aortic ECs with recombinant resistin increased monocyte chemoattractant protein (MCP)-1 and soluble vascular cell adhesion molecule (sVCAM)-1 protein levels in the conditioned medium.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16159596

Selventa

RAzK40JnlhJ0gBvojPv4y4MLyJikyjCuzxywxP6fqBe7c
has assertion: cat(p(HGNC:MSRA)) -| bp(GO:"response to oxidative stress")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.037+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:MSRA)) -| bp(GO:"response to oxidative stress")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16162094

4
value: MsrA (methionine sulphoxide reductase A) is an antioxidant repair enzyme that reduces oxidized methionine to methionine. Moreover, the oxidation of methionine residues in proteins is considered to be an important consequence of oxidative damage to cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16162094

Selventa

RA0sCDjZN5 rBtBuji2gnNYu4NDbUwSbsI3uWt0EVyH00
has assertion: tscript(p(HGNC:ATF5)) -> r(HGNC:ASNS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.087+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ATF5)) -> r(HGNC:ASNS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16164412

5
value: ATF5, a transcriptional activator, stimulates asparagine synthetase promoter/reporter gene transcription
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16164412

Selventa

RA2f7IcZaUlnC1jFx8niw7UMWTGuMJ4KwMo95DgZr9qQg
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:ADAM10)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.089+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:ADAM10)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA-6wlCrm1 Kct ktmKsIoBMUpWQmI3GTpVq9qJ 2ZrC0
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:COL18A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.106+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:COL18A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA5HouQYMBGZyMHB6UXNkdS7P ctXZWQ1AtGyxAAxd-10
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:COL7A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.108+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:COL7A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA83Xw1C85KQGHkqcxPTW3O7Xy73iwwF9xmgDQigIy4hw
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:HEPH)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.122+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:HEPH)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA7pOr9UwUonheyFMk s-nV5yEsiYlJdCJy-JQzXiNAug
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:IL13RA2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.127+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:IL13RA2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA821MFGwo9dlOfNl0FkXYdPK3h9Z T23GIE6684byq9E
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:MYBPC1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.138+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:MYBPC1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA5OkOVyqYAk2LlScBqPzc4lUbijvflezCGjruUs15H 4
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:MYLK)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.139+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:MYLK)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA NFubKagpTnUsCtl TTPBeNx3lomCKxAjil1n9Exkc
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:SPP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.146+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:SPP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA Lzav7z8Gj7g5LEYT0P6Lz 9bujdqyDN7GDY-Le6mV8
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:TNN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.154+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:TNN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA0nD1qQIHNxqomNkL6kWVWOyt uH1Gdv9u16Z8flxJdA
has assertion: path(MESHD:Fibrosis) positiveCorrelation r(HGNC:UBIAD1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.160+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Fibrosis) positiveCorrelation r(HGNC:UBIAD1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166619

3
value: TABLE 2. UPREGULATED GENES IN IDIOPATHIC PULMONARY FIBROSIS
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166619

Selventa

RA7nzyiGOCH73cV1MJyojdld2ifKuB24vXpOu4F1KS2iM
has assertion: cat(p(MGI:Sirt1)) =| tscript(p(MGI:Mef2d))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.166+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Sirt1)) =| tscript(p(MGI:Mef2d))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16166628

6
value: Instead, the NAD+-dependent deacetylase SIRT1 can potently induce MEF2 deacetylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16166628

Selventa

RA U9OTLu1IMHiEf44G2K4tTx cRWifXjRt4bjuUJlsSY
has assertion: bp(GO:"response to hypoxia") -| r(HGNC:KCNK5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.175+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| r(HGNC:KCNK5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16168386

3
value: Thus, we have cloned the TASK-2 promoter, demonstrated that its transcriptional activity is dependent upon pO(2), shown that deletion of overlapping consensus binding sites for NF-kappaB/Elk-1 ablates this O(2) sensitivity, and proved that Elk-1 binds preferentially to this site. Furthermore, the consequences of chronic hypoxia on natively expressed TASK-2 are decreased steady-state mRNA and cell depolarization showing that TASK-2 contributes to the excitability of this important lung cell type.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16168386

Selventa

RA2MUXzoHo86I87wj5Kka WQhFa0oqQCJzLGRNHwxkPc8
has assertion: p(HGNC:RAF1,pmod(P,S,621)) -> (p(PFH:"14-3-3 Family") =| kin(p(HGNC:RAF1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.213+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:RAF1,pmod(P,S,621)) -> (p(PFH:"14-3-3 Family") =| kin(p(HGNC:RAF1)))
label: p(PFH:"14-3-3 Family") =| kin(p(HGNC:RAF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

7
value: Phosphorylation. Raf is principally activated by phosphorylation of specific amino acid residues as shown for each isoform in Figure 4. From an evolutionary standpoint, the Raf activation sites are highly conserved from yeast to humans. Several amino acids in Raf, particularly serine (S) 259 and S621, which bind 14-3-3 and maintain C-Raf in a closed auto-inhibited conformation, are phosphorylated in the basal state.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RAyzwXx4lrUd5DCCvko7XxgTa LS4x-byIkv-3leYFVaw
has assertion: p(PFH:"RAS Family",pmod(F)) => gtp(p(PFH:"RAS Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.215+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFH:"RAS Family",pmod(F)) => gtp(p(PFH:"RAS Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

5
value: Raf may also be activated by Ras-independent elements and, in turn, propagates signals through diverse effectors that mediate proliferation, angiogenesis, metastases, and survival.5 Raf may be activated by signaling upstream or constitutively. Constitutive activation of Raf and Ras are indistinguishable in their potential to induce malignant transformation.6-8 Activating raf mutations have been identified in melanoma, thyroid, colon, and other cancers (Table 1).9-43 Furthermore, the disappointing clinical results of farnesyltransferase (FTase) inhibitors (FTIs) that were developed based on a flawed premise that they would effectively target malignancies with a high incidence of Ras mutation has led to scrutiny of signaling elements downstream of Ras, such as Raf, as therapeutic targets.44 This review highlights relevant information about the biology of Raf and novel strategies directed at exploiting this knowledge to more effectively treat malignant diseases. SIGNALING THROUGH THE MAPK PATHWAY The molecular mechanisms and signaling pathways that regulate cell proliferation and survival are receiving considerable attention as potential targets for anticancer strategies. 45,46 Recently, there has been a notable increase in efforts directed at targeting the MAPK pathway, which integrates a wide array of proliferative signals initiated by receptor tyrosine kinases (RTKs) and G protein- coupled receptors.47,48 The network of signals emanating from the MAPK pathway are transmitted by proteins that serve as chemical switches, cycling between phosphorylated (activated) and dephosphorylated (inactivated) states.49 These on and off switches are regulated by kinases and phosphatases, respectively. Activated signaling elements, in turn, phosphorylate amino acid residues on downstream signaling proteins in a cascade-like and expansive manner.50 Not only does the centrality of the MAPK pathway render its components important targets for therapeutic development, but many genes tha[cell cut: 3950 characters, first 2000 kept]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RA0jmg5sYPSnevhCqcADAEnBOIoyuPQ36xgCkZzEC9o2A
has assertion: gtp(p(HGNC:RHOD)) -> kin(p(HGNC:ROCK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.221+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:RHOD)) -> kin(p(HGNC:ROCK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

6
value: The Rho family of small GTPases, consisting of Rho, Rac, and cyclin-dependent kinase (Cdc) 42, regulate cytoskeletal organization during the cell cycle and also mediate Ras-induced activation of Raf, especially C-Raf.134-136 These GTPases do not directly bind to Raf but, instead, signal by activating downstream kinases. Rho signals by activating the serine/threonine protein kinases N1 and N2 and Rho-associated kinase 1, whereas Rac and Cdc42 signal through p21-activated kinase (PAK).134-136
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RAxZ6KOtEKBluUNTbbKV4G4F9ta4lBMkPX5U4JzIKzqmg
has assertion: kin(p(HGNC:RAF1)) => p(HGNC:BCL2,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.228+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RAF1)) => p(HGNC:BCL2,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

5
value: This action releases activated NF-kB, which is then translocated to the nucleus where it mediates transcription of antiapoptotic factors.155,166 Other antiapoptotic effects of C-Raf are mediated by a mitochondrial pool of the protein, which, on stimulation, localizes to the mitochondrial membrane where the protein interacts with and phosphorylates Bcl-2, Bcl-2-associated athanogene, and other pro-apoptotic regulators, abrogating their pro-apoptotic effects.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RA8LkR7ioGZbdZ4T-i2B6Lx-0-y4x6VMckoYPGgcGhYng
has assertion: kin(p(HGNC:RAF1)) => cat(p(HGNC:BCL2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.229+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RAF1)) => cat(p(HGNC:BCL2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

6
value: This action releases activated NF-kB, which is then translocated to the nucleus where it mediates transcription of antiapoptotic factors.155,166 Other antiapoptotic effects of C-Raf are mediated by a mitochondrial pool of the protein, which, on stimulation, localizes to the mitochondrial membrane where the protein interacts with and phosphorylates Bcl-2, Bcl-2-associated athanogene, and other pro-apoptotic regulators, abrogating their pro-apoptotic effects.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RAwHkqHNrdvQ5115-E3Q2ocYH8hfV7bcFusgFqij b 3M
has assertion: p(HGNC:EPO) -> p(HGNC:RAF1,pmod(P,Y,341))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.231+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EPO) -> p(HGNC:RAF1,pmod(P,Y,341))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

4
value: Y341 is phosphorylated by the Src family of non-RTKs, Janus kinase, and erythropoietin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RAzej4px6q9qvN5tkoVJ5loZ8X8L5NXnwpUceB2tLZ1XI
has assertion: kin(p(PFH:"PRKA Family")) =| kin(p(HGNC:RAF1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.234+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) =| kin(p(HGNC:RAF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

6
value: and phosphorylation by protein kinases A (PKA) and B (PKB/Akt),
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RA2Po1N9Bca4uBSe6LSbT74gKypID-lVRVoDhYmuOIUXc
has assertion: a(SCHEM:"cyclic AMP") -> (gtp(p(HGNC:RAP1A)) -> kin(p(HGNC:RAF1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.236+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -> (gtp(p(HGNC:RAP1A)) -> kin(p(HGNC:RAF1)))
label: gtp(p(HGNC:RAP1A)) -> kin(p(HGNC:RAF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170185

7
value: as shown in Figure 2.95-98 In essence, the activation status of Raf depends on the integration of both activating and inhibitory stimuli, the net result of which determines the downstream messages. THE RAF FAMILY OF GENES AND PROTEINS The raf family of genes was first identified as oncogenes in retroviruses that are the causative vectors of tumors in mice and chicken.99,100 The first raf gene to be identified, v-raf, the transforming gene of the mouse sarcoma virus 3611, induces fibrosarcomas and erythroleukemia in newborn mice, and C-raf (also called raf-1) is its proto-oncogene homolog.101,102 A-raf was found next by screening a mouse spleen cDNA library at low stringency with a v-raf probe. Next, v-Rmil was identified as the transforming gene in the avian retrovirus Mill Hill No. 2 (MH2) from a spontaneous ovarian tumor and found to be homologous to v-raf.99 C-Rmil corresponded to a third mammalian raf gene, B-raf, which was also shown to be an oncogene.103,104 However, initial attempts to identify activated versions of raf in human cancers failed to demonstrate unique DNA rearrangements in any specific tumor type, which, in retrospect, can be attributed to the lack of requisite sensitivity of early assays to detect single point mutations. Furthermore, most early efforts were directed at C-raf, rather than at the more oncogenic B-raf. The mammalian raf family consists of the following three genes: A-raf, B-raf, and C-raf, which are located on chromosomes Xp11, 7q32, and 3p25, respectively. The raf proto-oncogenes encode three 68- to 74-kd cytosolic proteins, termed A-Raf, B-Raf, and C-Raf (Raf-1), which share highly conserved amino-terminal regulatory regions and catalytic domains at the carboxyl terminus (Fig 4).10 As serine/threonine kinases, Raf proteins phosphorylate serine and threonine residues on essential modulatory proteins downstream of Ras. Each Raf species has a distinct expression profile in tissues, which suggests that individual Raf isoforms perfor[cell cut: 3941 characters, first 2000 kept]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170185

Selventa

RAzDwQmAWwPk6EC0u-KbRU0Qxfd7FN0R5qNMX8r4bnKNs
has assertion: p(HGNC:EGF) -> kin(p(PFH:"MAPK p38 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.246+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> kin(p(PFH:"MAPK p38 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170353

5
value: senescence-like growth arrest was accompanied by impaired activation of mitogen-activated protein kinase (MAPK) pathways, namely, extracellular-regulated protein kinase, c-jun N-terminal kinase and p38 MAPK, in response to epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170353

Selventa

RA5S5xBbgjDP3HjHt5GR yvzuqKnKcnV53TGlI8-Teyvg
has assertion: cat(p(HGNC:SIRT1)) -> (p(HGNC:IGF1) -> kin(p(PFH:"MAPK Erk1/3 Family")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.254+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SIRT1)) -> (p(HGNC:IGF1) -> kin(p(PFH:"MAPK Erk1/3 Family")))
label: p(HGNC:IGF1) -> kin(p(PFH:"MAPK Erk1/3 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16170353

8
value: senescence-like growth arrest was accompanied by impaired activation of mitogen-activated protein kinase (MAPK) pathways, namely, extracellular-regulated protein kinase, c-jun N-terminal kinase and p38 MAPK, in response to epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16170353

Selventa

RA-sE euNA09ZwtWpvYJOaeqMzqTyKAujTqA0gOy3SgPg
has assertion: cat(p(HGNC:PTGS2)) -> a(SCHEM:"15-deoxy-D12,14-prostaglandin J2")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.264+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:PTGS2)) -> a(SCHEM:"15-deoxy-D12,14-prostaglandin J2")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16172382

4
value: COX-2 inhibitors...in the vasculature prevents the accumulation of COX-2- derived 15d-PGJ2, which is associated with the atheroprotective nature of laminar flow.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16172382

Selventa

RAwh8o 0EppGLWLhKHgBuZGOFNDrnVilySFUHuyipJsbo
has assertion: path(SDIS:"acute phase reaction") -| r(RGD:Cebpa)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.266+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"acute phase reaction") -| r(RGD:Cebpa)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16172914

3
value: The AP reaction was accompanied by a decrease of the relative concentration of C/EBP alpha and an increase of C/EBP beta
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16172914

Selventa

RA8LbvZRPP-kc6xwHgFM X60b80Q5KKHzeDtJUE7eH58M
has assertion: p(HGNC:CD28) -> p(HGNC:DOK1,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.273+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CD28) -> p(HGNC:DOK1,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177091

4
value: CD2 or CD28 stimulation, but not CD3/TCR stimulation, induces Dok phosphorylation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177091

Selventa

RA8JNlBEM VJ4Jxpu1TD86J3BLaKaZET8R2Bj0Jvoc2UY
has assertion: path(SDIS:"Type I diabetes") positiveCorrelation p(HGNC:CSF2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.274+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"Type I diabetes") positiveCorrelation p(HGNC:CSF2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177100

3
value: Unstimulated monocytes of at-risk/type 1 diabetic humans and macrophages of the NOD mouse have markedly elevated autocrine GM-CSF production and persistent STAT5 phosphorylation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177100

Selventa

RA2RsrJyojVw9tDdYLEe0 -IaxdFbNOWKywixmWYqaWbo
has assertion: a(SCHEM:"serum insulin") -| a(SCHEM:"cyclic AMP")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.278+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -| a(SCHEM:"cyclic AMP")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177793

2
value: Acute insulin treatment activates phosphodiesterase 3B, reduces cAMP levels and quenches beta-adrenergic receptor signalling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177793

Selventa

RA17Agj1JYTmZcjt x5cljCK3gdMhUQFbGKl9zOECG5uE
has assertion: a(SCHEM:"serum insulin") -| cat(p(PFH:"ADRB Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.282+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -| cat(p(PFH:"ADRB Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177793

4
value: Acute insulin treatment activates phosphodiesterase 3B, reduces cAMP levels and quenches beta-adrenergic receptor signalling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177793

Selventa

RAzD1Ds fCrjHGIoGWCfINv64Kuzu97tx6499qy5sc5GA
has assertion: cat(p(HGNC:ADRB2)) -> a(SCHEM:"cyclic AMP")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.295+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:ADRB2)) -> a(SCHEM:"cyclic AMP")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177793

4
value: In adipocytes, stimulation of beta-adrenergic receptors increases cyclic AMP levels and activates protein kinase A (PKA), which stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177793

Selventa

RA8uFw7xkjuWCVp69IVnOgvBwv1U1ajeQf-XL-JMYSP3Y
has assertion: kin(p(PFH:"PRKA Family")) -> p(EGID:5346,pmod(P,S))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.301+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) -> p(EGID:5346,pmod(P,S))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177793

5
value: In adipocytes, stimulation of beta-adrenergic receptors increases cyclic AMP levels and activates protein kinase A (PKA), which stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177793

Selventa

RA-mvooYubl3ptFMLzdm9444XwY-nguhyEaWH2uh5HIvo
has assertion: kin(p(PFH:"PRKA Family")) -> path(SDIS:"adipocyte lipolysis")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.302+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKA Family")) -> path(SDIS:"adipocyte lipolysis")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16177793

4
value: In adipocytes, stimulation of beta-adrenergic receptors increases cyclic AMP levels and activates protein kinase A (PKA), which stimulates lipolysis by phosphorylating hormone-sensitive lipase and perilipin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16177793

Selventa

RA37cETEYHNwNBjfGvXBSo31fHJq2Q8dFjtHXOvy89FxY
has assertion: tscript(p(HGNC:E2F8)) -| tscript(p(PFH:"E2F Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.313+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:E2F8)) -| tscript(p(PFH:"E2F Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16179649

6
value: The E2F family of transcription factors are downstream effectors of the retinoblastoma protein, pRB, pathway and are essential for the timely regulation of genes necessary for cell-cycle progression. Here we describe the characterization of human and murine E2F8, a new member of the E2F family. Sequence analysis of E2F8 predicts the presence of two distinct E2F-related DNA binding domains suggesting that E2F8 and, the recently, identified E2F7 form a subgroup within the E2F family. We show that E2F transcription factors bind the E2F8 promoter in vivo and that expression of E2F8 is being induced at the G1/S transition. Purified recombinant E2F8 binds specifically to a consensus E2F-DNA-binding site indicating that E2F8, like E2F7, binds DNA without the requirement of co-factors such as DP1. E2F8 inhibits E2F-driven promoters suggesting that E2F8 is transcriptional repressor like E2F7. Ectopic expression of E2F8 in diploid human fibroblasts reduces expression of E2F-target genes and inhibits cell growth consistent with a role for repressing E2F transcriptional activity. Taken together, these data suggest that E2F8 has an important role in turning of the expression of E2F-target genes in the S-phase of the cell cycle.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16179649

Selventa

RAy9WApXJPdRur5TIaLNEEJ2cH46BC7Kj1slfswELGnrI
has assertion: tscript(p(HGNC:HBP1)) -> r(HGNC:FASLG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.316+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:HBP1)) -> r(HGNC:FASLG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16179914

5
value: Fas ligand mRNA levels were increased in HBP1 transfectants, suggesting involvement of the Fas/Fas ligand pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16179914

Selventa

RA K6 7D6WO7KA8fodc9poDFPS2RgWMfrHxEITErCoCN0
has assertion: p(MGI:Ereg) -| r(MGI:Il18)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.322+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Ereg) -| r(MGI:Il18)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/16182244

4
value: rmEP reduced IL-18 expression in WT- and EP –/–-derived keratinocytes at 8 h after stimulation, and there was no obvious difference between WT and EP –/– (Fig. 3D).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/16182244

Selventa

RAybbDZRcZe3aqUmDKWdO-VdCR6mIY9gEgPRNuu0kagnY
has assertion: assertion
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:38.323+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234