RAJzDsKLR-XgFp3BKFnGRU6t1g2tR8m o047fJBpASgnw
has assertion: a(CHEBI:"angiotensin II") -| r(MGI:Pln)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.706+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -| r(MGI:Pln)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

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 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RANeohhArUk62kwXoKVqwB1ln6ttnXOmoA68Fqa6CUizw
has assertion: a(CHEBI:"angiotensin II") -| r(MGI:Sdhd)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.709+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -| r(MGI:Sdhd)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAMYCYLQxSNiiO1KW1lEuVxaO xadupwiEOvnKtzi3Csk
has assertion: a(CHEBI:"angiotensin II") -| r(MGI:Slc25a4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.710+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -| r(MGI:Slc25a4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAFXtxRraz3DJbeNOlCwjq8M9jDL0IE7kG9oJbdgQ68EU
has assertion: a(CHEBI:"angiotensin II") -| r(MGI:Uqcrfs1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.714+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -| r(MGI:Uqcrfs1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAFog85BSRJoJ pRaxpphLO0E9Q3qNVmHUd6Zv5mA-nPA
has assertion: a(CHEBI:"angiotensin II") -> r(MGI:Col3a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.724+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -> r(MGI:Col3a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAE8nZQRCPp9ick-eFaBCki8PTEJENcqoHMDcM-O3D3qw
has assertion: a(CHEBI:"angiotensin II") -> r(MGI:Rpl39)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.741+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -> r(MGI:Rpl39)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAM6bJx09pOVnOmjwH4RY6hs-YFQc10SI9TrB51AHj4gE
has assertion: a(CHEBI:"angiotensin II") -> r(MGI:Reep5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.742+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -> r(MGI:Reep5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RAJhTRCs2k CD9aD-6gaaS2jYp4kMKK7ULNrY-1qw2hWQ
has assertion: a(CHEBI:"angiotensin II") -> r(MGI:Rpl4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.744+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"angiotensin II") -> r(MGI:Rpl4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15242839

3
value: Table 2. Differentially expressed genes identified by SAGE
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15242839

RALnlJMiTPWFWSfgVkrTTay3Fn5zu3kctBv7H8OadOfvo
has assertion: bp(GO:aging) -> r(HGNC:RARA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.767+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:RARA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15246741

3
value: We found that intrinsic ageing of skin in vivo is accompanied by significant increases of RAR alpha mRNA and protein
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15246741

RAJOkpPPMTymjKiPQ7qocfSkqo4CIlZoZFB50xZ Ogo7Y
has assertion: a(SCHEM:"cyclic AMP") -| kin(p(HGNC:MAPK14))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.774+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -| kin(p(HGNC:MAPK14))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15246972

4
value: Our data demonstrate that increased intracellular cAMP concentration in endothelial cells prevents thrombin-induced ICAM-1 expression by inhibiting p38 MAPK activation, which in turn prevents phosphorylation of RelA/p65 and transcriptional activity of the bound NF-kappaB.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15246972

RAEBluJVrL6W0NTKMj-BlLTRvQbBcQNII6dDc1y0Q3774
has assertion: p(PFH:"VEGF Family") -> p(HGNC:PTK2,pmod(P,Y,407))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.777+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFH:"VEGF Family") -> p(HGNC:PTK2,pmod(P,Y,407))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247219

4
value: Exposure of endothelial cells to vascular endothelial growth factor (VEGF) induced tyrosine phosphorylation of focal adhesion kinase (FAK) on site Tyr(407), an effect that required the association of VEGF receptor 2 (VEGFR2) with HSP90.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247219

RAJzyV9O1kIbuf-mgbWNuU3zKjSDZQ1oBWfhtsD578bno
has assertion: kin(p(HGNC:SRC)) -> complex(p(HGNC:VCL),p(HGNC:PTK2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.786+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:SRC)) -> complex(p(HGNC:VCL),p(HGNC:PTK2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247219

7
value: We also found that the recruitment of paxillin to FAK was inhibited by geldanamycin but not by PP2, whereas both geldanamycin and PP2 inhibited the recruitment of vinculin to FAK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247219

RAMFuSbd kZeRVqLsArxY94tlLF2xwHoOTTe7Y7MlJBNI
has assertion: a(SCHEM:Estrogens) -> r(HGNC:EGLN2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.789+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Estrogens) -> r(HGNC:EGLN2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247232

3
value: Thus in different cell types, isoform-specific patterns of PHD induction by hypoxia and estrogen alter both the relative abundance of the PHDs and their relative contribution to the regulation of HIF.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247232

RAKBgOqdYAV2fsQ0jDsgEBEYlQ zygzoIJOG8BVHghcgc
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:EGLN3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.794+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:EGLN3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247232

3
value: Thus in different cell types, isoform-specific patterns of PHD induction by hypoxia and estrogen alter both the relative abundance of the PHDs and their relative contribution to the regulation of HIF.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247232

RAJVLgvgw2V3P4yPvkKANBwB s2h a nUuJYblt-I-cBk
has assertion: p(EGID:3630) -> surf(p(HGNC:SLC2A4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.799+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:3630) -> surf(p(HGNC:SLC2A4))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247266

5
value: Insulin stimulates glucose transport in muscle and adipose tissues by recruiting intracellular membrane vesicles containing the glucose transporter GLUT4 to the plasma membrane.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247266

RAItgD8n6MtTVcXomRV6877n20rCLfWDdsRS0TwIfKgw8
has assertion: p(EGID:3630) -> surf(p(HGNC:SLC2A4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.800+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:3630) -> surf(p(HGNC:SLC2A4))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247266

5
value: Insulin stimulates glucose transport in muscle and adipose tissues by recruiting intracellular membrane vesicles containing the glucose transporter GLUT4 to the plasma membrane.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247266

RAG8iz90jEOIz1A0flcP7XWHKOdK-IjBvdky7fZS9FL7Y
has assertion: kin(p(MGI:Src)) => p(MGI:Dapp1,pmod(P,Y,139))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.812+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) => p(MGI:Dapp1,pmod(P,Y,139))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247305

5
value: The positive and negative effects of Bam32 variants on F-actin levels were closely mirrored by their effects on the activation of the GTPase Rac1, which is known to regulate actin remodeling in lymphocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247305

RAEVseKSDwIMwh4MSi4DyUflhYFL0oC6fdB84pXlX9rew
has assertion: cat(p(MGI:Cyb5r4)) -| p(EGID:16847)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.816+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Cyb5r4)) -| p(EGID:16847)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15247412

5
value: Thus, the Ncb5or -/- animals have a rather pure diabetic/fat phenotype.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15247412

RANEkg-FnLaIpGoJRyG0igGeR3srsLhbcNAx1YM0V4n 8
has assertion: kin(p(MGI:Rps6kb1)) -| bp(GO:"cell growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.831+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Rps6kb1)) -| bp(GO:"cell growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15249583

4
value: The tuberous sclerosis complex (TSC1-2) suppresses cell growth by negatively regulating a protein kinase, p70S6K (S6K1), which generally requires PI3K signals for its activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15249583

RAPNGaiMDcCCazHuB-dQ8aR Ruf5wX1Tcmo2IQG2suoZo
has assertion: cat(p(HGNC:AKR1B1)) -> tscript(complex(NCH:"AP-1 Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.843+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AKR1B1)) -> tscript(complex(NCH:"AP-1 Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15251463

5
value: Inhibition of AR by sorbinil or tolrestat prevented TNF-alpha-induced increase in Bax and Bak and the downregulation of Bcl-2. Inhibition of AR abrogated AP-1 DNA binding activity and prevented the activation of caspase-3, JNK, and p38 MAPK in cells stimulated by TNF-alpha. Exposure to TNF-alpha also induced apoptotic cell death, which was attenuated by AR inhibition or antisense ablation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15251463

RAMG53xh8LdN0pIHKmL d67UPeg3O6qF36jx1aQZcgSKM
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:ID2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.846+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:ID2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15252039

3
value: ID (inhibitor of differentiation/DNA binding) proteins, frequently deregulated in advanced human malignancies, can participate in multiple fundamental traits of cancer, such as block of differentiation, increased proliferation, tissue invasiveness, and angiogenesis. We have previously demonstrated that hypoxia decreases expression of neuronal marker genes in neuroblastoma, but induces genes expressed in the neural crest, such as ID2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15252039

RAM4wumVDhgzaDrmnGoIT4IMQCnXSDQ8-s2Az8cwlpDxc
has assertion: tscript(p(MGI:Pou4f1)) -| r(MGI:Ankrd1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.850+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -| r(MGI:Ankrd1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 1. Increased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAHiY55eBV6-hlC3P P77v6v5xIuZ nRaaOJ-JaYELMKo
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Anxa2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.882+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Anxa2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RALX S54iY4x-Qm5X--3PAZdHHXlWAgrV1hnfEafuN-94
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Apoe)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.885+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Apoe)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAGyGstfW6AMw2InXkJ2E86dA2XAOzID uN g Aalaey8
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Bnc1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.887+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Bnc1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAJtZEkqKMuGeWcQtxW5RUEIHl5XNem-hoL7HyUy81zxc
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Fgf13)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Fgf13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAPyUBMwm1-aCimXpF8jtmRC8stky75tRvDBptwFYMXGo
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Hmx1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.895+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Hmx1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAJtaqAbiT-gsb6E5AOWtlI8h3E0BWYnRWBYIIv1gb5Q8
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Lxn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.904+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Lxn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAHMBTLGmjOs9Fd8qlq7os7Ar95lENrS2w184wmp-cx9A
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Olfm1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.908+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Olfm1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RALSqwcghb4OGbetu2O7EMJ4S9ZBTfBmjmEqaTNOVLgLg
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Scn7a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.917+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Scn7a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAH9mnKltXx5HTiC3-rlHTP2RwMAfN3xhbth5579FBV3M
has assertion: tscript(p(MGI:Pou4f1)) -> r(MGI:Slc4a4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.920+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pou4f1)) -> r(MGI:Slc4a4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253936

5
value: Table 2. Decreased transcripts in the trigeminal ganglion of Brn3a mutant mouse embryos
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253936

RAMyZzaxTBCCvFvPVX5t3q-hiismJqqyjAZN4JTsdIO0U
has assertion: p(HGNC:SPRY2) -| kin(p(PFH:"MAPK p38 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.924+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SPRY2) -| kin(p(PFH:"MAPK p38 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15253939

5
value: FGF signaling is both necessary and sufficient for their expression By contrast, Mkp3, Sef and Spry act within cells as negative feedback inhibitors, modulating and restricting the levels and extent of FGF signaling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15253939

RANPLJVu6fsmOBIHQJcV6QVO9wt6qnBXvoBv5ObPprIXM
has assertion: p(HGNC:MTA1) -| tscript(p(HGNC:ESR1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.928+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MTA1) -| tscript(p(HGNC:ESR1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15254226

5
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15254226

RAMWXxqvxEloJ47OXvKx2E90APJRoI8jW5xOsZkH1 6gE
has assertion: p(HGNC:EPO) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.930+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EPO) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15254422

4
value: FROM FULL TEXT: Both Epo and SCF (Kitl) recruit and activate PI3k
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15254422

RALNHOU1PyCuh6xuI6jiWj1e qUPyfgelhGzzHiciNGzY
has assertion: p(RGD:Retn) -| kin(complex(NCR:"AMP Activated Protein Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.939+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Retn) -| kin(complex(NCR:"AMP Activated Protein Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15254589

4
value: Resistin causes defective AMPK activation in response to insulin. Since AMPK signaling affects insulin-sensitive glucose metabolism (19 22) and since AMPK can act upstream of Akt signaling (23, 24), we assessed whether resistin overexpression alters AMPK activity. As demonstrated in Figure 7, AMPK phosphorylation (Thr172) was reduced by 60%, 35%, and 64% (P 0.01) in the skeletal muscle, adipose tissue, and liver of rats injected with Adv-resistin, respectively, while AMPK protein content remained unchanged.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15254589

RAH8znVhwDII6jENN7slZdoVFCOvtuNV0tQFaXH8BSmkM
has assertion: kin(p(HGNC:IGF1R)) -> path(SDIS:"tumor growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.946+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:IGF1R)) -> path(SDIS:"tumor growth")
label: p(HGNC:INTS6) -| (kin(p(HGNC:IGF1R)) -> path(SDIS:"tumor growth"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15254679

6
value: These results demonstrate that DICE1 has a growth-suppressing activity and interferes with anchorage-independent growth of IGF-IR transformed tumor cells dependent upon IGF-I signaling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15254679

RAEfb43Cba 7m6BxdGPLFmWbbm38MI8FRA1pOXyiBk-WM
has assertion: cat(p(HGNC:P2RY6)) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:25.957+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:P2RY6)) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15254971

4
value: We found that P2Y6 activation controlled cell proliferation but not the activity of the Na+/K+ATPase.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15254971

RAMXvbcgNfKTTgQiU-snEIT6Ydlw66RWJos0yAcd5r2ys
has assertion: kin(p(MGI:Stk11)) -| p(MGI:Eif4ebp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.012+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Stk11)) -| p(MGI:Eif4ebp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15261145

5
value: LKB1-deficient tumors are shown here to exhibit elevated levels of S6K1 activity and phospho-4EBP1, indicative of hyperactivation of mTOR signaling
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15261145

RAHfC0EmBV55Ps1QzCC-3PknrC-mqoWQPj0A0hYRHXD88
has assertion: phos(complex(NCH:"Calcineurin Complex")) -> r(HGNC:RCAN1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.027+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(complex(NCH:"Calcineurin Complex")) -> r(HGNC:RCAN1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15263820

4
value: VEGF-stimulated induction of DSCR1 was blocked by anti-VEGF receptor-2 monoclonal antibody (mAb), or the specific calcineurin inhibitors cyclosporin A and FK506.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15263820

RAJ saFkms7qDiViwJCJ6Hcqxr9ua-5435EW6SbP5-N00
has assertion: a(CHEBI:"gamma-aminobutyric acid") -> p(RGD:Fgf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.033+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"gamma-aminobutyric acid") -> p(RGD:Fgf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15264218

3
value: Histamine, glutamate, carbachol, serotonin or gamma-aminobutyric acid (GABA) caused an increase of FGF-1 content
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15264218

RAFjbzJ6CYF7z7b-FZWXpILuEc Sfy5h jVIEOOT2Z5KU
has assertion: cat(p(PFR:"Adrb Family")) -| r(RGD:Fgf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.035+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(PFR:"Adrb Family")) -| r(RGD:Fgf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15264218

5
value: This mechanism was proved to function in vivo by stimulation of FGF-1 expression in neurons of the cerebral cortex after intracerebral administration of propranolol, an antagonist of adrenergic beta receptors
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15264218

RAFC7T4CkNA4K2MM2qjIAeNOSNbvx 5tgF-4IT2PePWW4
has assertion: p(HGNC:IL3) -> p(HGNC:IL4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.044+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL3) -> p(HGNC:IL4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

4
value: The IL-3-induced generation of IL-4, IL-13 and histamine was inhibited to a statistically significant (P<0.05) extent, only by compounds that act as inhibitors of PDE4.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RAFRLM7rAD5z3IWzBwpPhG8m-CZqq97ScJt15UlGcQJLA
has assertion: a(SCHEM:"Org 30029") -| (p(HGNC:IGHE) -> p(HGNC:IL4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.060+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Org 30029") -| (p(HGNC:IGHE) -> p(HGNC:IL4))
label: p(HGNC:IGHE) -> p(HGNC:IL4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

5
value: The effects of the isoform-selective inhibitors, 8-methoxymethyl-IBMX (PDE 1 inhibitor), siguazodan (PDE3 inhibitor), rolipram (PDE4 inhibitor), denbufylline (PDE4 inhibitor), Org 30029 (mixed PDE3 and 4 inhibitor) and zaprinast (PDE5 inhibitor), were studied. Of these selective compounds, only rolipram, denbufylline and Org 30029 inhibited the IgE-dependent generation of IL-4, IL-13 and histamine from basophils
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RAOeZL41TD7DssrJFUoz7RbxYiu8bTA1xRJbwIYDaxEro
has assertion: a(CHEBI:rolipram) -| (p(HGNC:IGHE) -> p(HGNC:IL4))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.062+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:rolipram) -| (p(HGNC:IGHE) -> p(HGNC:IL4))
label: p(HGNC:IGHE) -> p(HGNC:IL4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

5
value: The effects of the isoform-selective inhibitors, 8-methoxymethyl-IBMX (PDE 1 inhibitor), siguazodan (PDE3 inhibitor), rolipram (PDE4 inhibitor), denbufylline (PDE4 inhibitor), Org 30029 (mixed PDE3 and 4 inhibitor) and zaprinast (PDE5 inhibitor), were studied. Of these selective compounds, only rolipram, denbufylline and Org 30029 inhibited the IgE-dependent generation of IL-4, IL-13 and histamine from basophils
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RALvWSLgCIfzI-i3EU7O2WLux-o6Wi qzu-RwW6jLLGZk
has assertion: cat(p(PFH:"PDE4 Family")) -> (p(HGNC:IGHE) -> p(HGNC:IL13))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.064+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(PFH:"PDE4 Family")) -> (p(HGNC:IGHE) -> p(HGNC:IL13))
label: p(HGNC:IGHE) -> p(HGNC:IL13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

7
value: The effects of the isoform-selective inhibitors, 8-methoxymethyl-IBMX (PDE 1 inhibitor), siguazodan (PDE3 inhibitor), rolipram (PDE4 inhibitor), denbufylline (PDE4 inhibitor), Org 30029 (mixed PDE3 and 4 inhibitor) and zaprinast (PDE5 inhibitor), were studied. Of these selective compounds, only rolipram, denbufylline and Org 30029 inhibited the IgE-dependent generation of IL-4, IL-13 and histamine from basophils
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RAKuRK2smP3rwu-HPALo2x9v64G7JvQNOPQU1uNWduu-w
has assertion: a(SCHEM:"1-Methyl-3-isobutylxanthine") -| (p(HGNC:IGHE) -> p(HGNC:IL13))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.067+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"1-Methyl-3-isobutylxanthine") -| (p(HGNC:IGHE) -> p(HGNC:IL13))
label: p(HGNC:IGHE) -> p(HGNC:IL13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

5
value: The nonselective PDE inhibitors, isobutyl-methylxanthine (IBMX) and theophylline, attenuated the IgE-mediated generation of IL-4 and IL-13 and, also, the release of histamine from basophils.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RAI0oSJDhayQ3qHfaMGXJS7-lB sDCeAAEfXGvJIdr06Q
has assertion: a(CHEBI:theophylline) -| (p(HGNC:IGHE) -> p(HGNC:IL13))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.073+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:theophylline) -| (p(HGNC:IGHE) -> p(HGNC:IL13))
label: p(HGNC:IGHE) -> p(HGNC:IL13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15265810

5
value: The nonselective PDE inhibitors, isobutyl-methylxanthine (IBMX) and theophylline, attenuated the IgE-mediated generation of IL-4 and IL-13 and, also, the release of histamine from basophils.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15265810

RANTlGRIgfj9WH8zN7WZJ6Wvn4vAuIn0V9JwzCj3ltk I
has assertion: cat(p(HGNC:NOS3)) => a(CHEBI:"nitric oxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.084+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:NOS3)) => a(CHEBI:"nitric oxide")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15269335

4
value: OS exists in three distinct isoforms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive isoforms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15269335

RALDmYFe3wQk GHnHfiNRKWx0a9hn6zCj43VVdj4M4qKo
has assertion: a(SCHEM:Isoproterenol) -> sec(p(PFR:"Ldh Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.088+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Isoproterenol) -> sec(p(PFR:"Ldh Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15271422

4
value: Isoproterenol (150 mg kg(-1) intraperitonially twice at an interval of 24 h) caused increase in the levels of serum marker enzymes via creatinekinase (CK), creatinekinase-MB (CK-MB) isoenzyme, lactatedehydrogenase (LDH) and lactatedehydrogenase isoenzyme (LDH1).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15271422

RAKZL7RVKzr2q L4p18O1b lo4i5PYoeGjknMPMvsETo
has assertion: a(SCHEM:"cyclic AMP") -> sec(p(RGD:Ckm))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.089+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -> sec(p(RGD:Ckm))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15271422

4
value: Isoproterenol (150 mg kg(-1) intraperitonially twice at an interval of 24 h) caused increase in the levels of serum marker enzymes via creatinekinase (CK), creatinekinase-MB (CK-MB) isoenzyme, lactatedehydrogenase (LDH) and lactatedehydrogenase isoenzyme (LDH1).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15271422

RAIzwFWHxi08jr912tQ8LLSBL-iRnetaVtj0JHBwPs-Bg
has assertion: p(HGNC:UACA) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.096+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:UACA) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15271982

3
value: We show here that Nucling was up-regulated by proapoptotic stimuli and important for the induction of apoptosis after cytotoxic stress. We further demonstrated that overexpressed Nucling was able to induce apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15271982

RAO riECbQPBN3YpXfovd12PcJbyzlfLw19uYjdzfNwNo
has assertion: tscript(p(MGI:Foxo1)) -> r(MGI:Alb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.097+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -> r(MGI:Alb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: Supplemental information 1 Increased gene expression in the skeletal muscle of FOXO1 mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAIo VQ AKS8cDQYY2L5vmCRk5monSZbNApLqafJ3jEOI
has assertion: tscript(p(MGI:Foxo1)) -> r(MGI:Cdkn1c)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.099+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -> r(MGI:Cdkn1c)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: Supplemental information 1 Increased gene expression in the skeletal muscle of FOXO1 mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAEWd2vGBNPrm87CeI2YzRE4-AqwEyO6gcHGsg9WNI LM
has assertion: tscript(p(MGI:Foxo1)) -> r(MGI:Gadd45g)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.100+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -> r(MGI:Gadd45g)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: Supplemental information 1 Increased gene expression in the skeletal muscle of FOXO1 mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RALh3ZS jBYjwmtfhbbR TjR3mx3hPkBuJLDoGG6F Ngk
has assertion: tscript(p(MGI:Foxo1)) -| r(MGI:Dmpk)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.114+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -| r(MGI:Dmpk)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: TABLE II - Gene with decreased expression in the skeletal muscle of FOXO1 mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAE3ADOVPt1PODco1y9riwGNS4Xv4wlJ5VL0fdIFuHndQ
has assertion: tscript(p(MGI:Foxo1)) -| r(MGI:Pla2g7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.123+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -| r(MGI:Pla2g7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: TABLE II - Gene with decreased expression in the skeletal muscle of FOXO1 mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAEFA-MLBRIVaHVn0mhov1hXlUZFgZfD2CEw2sH4eR7kQ
has assertion: tscript(p(MGI:Foxo1)) -| r(MGI:Tnnt1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.124+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -| r(MGI:Tnnt1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: TABLE II - Gene with decreased expression in the skeletal muscle of FOXO1 mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAJeXql4q 8V3Dgffeg0zsFUjEvabIpxyJp4QKPmub6t8
has assertion: tscript(p(MGI:Foxo1)) -| r(MGI:Ube2e1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.130+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxo1)) -| r(MGI:Ube2e1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15272020

5
value: TABLE II - Gene with decreased expression in the skeletal muscle of FOXO1 mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15272020

RAPthvPR6qxAuI3mEd--sOzjCt5cMW pRdIrcSXZxuQ58
has assertion: p(HGNC:CUL1) -| p(HGNC:CDKN2A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.134+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CUL1) -| p(HGNC:CDKN2A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15273726

4
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15273726

RAEWXAq7C4WQiIqAeFbFP0M46pRH3pheiV3 HRDDo7Nj8
has assertion: a(SCHEM:Estrogens) -> r(MGI:Tff1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.167+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Estrogens) -> r(MGI:Tff1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15282304

3
value: RIZ1 is an estrogen receptor (ER) coactivator but is also a histone lysine methyltransferase that methylates lysine 9 of histone H3, an activity known to repress transcription
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15282304

RAKw4dby3zqoAfYxYPve3lnrnvEI4mhq1qg3TtZum1ESU
has assertion: a(CHEBI:"okadaic acid") -> kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.186+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"okadaic acid") -> kin(p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15283964

4
value: We upregulated Akt activity using two experimental models: treatment with a protein phosphatase inhibitor, okadaic acid
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15283964

RAP9axQK0yakOB6oz8YZoyOnQ4lkSkLYRB9F9gYDmonNo
has assertion: a(SCHEM:"SC 58125") -| cat(p(MGI:Ptgs2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.192+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"SC 58125") -| cat(p(MGI:Ptgs2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284181

4
value: To confirm that COX-2 was the source of peroxides in the K-rasV12 transfected cells, we treated the cells with COX-2- specific inhibitor, SC58125.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284181

RAJVOxQxTtG8sLIMmGL11mSAQj0gqZaXuOs AqnSTsFUQ
has assertion: a(SCHEM:"cyclic AMP") -> r(HGNC:AREG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.196+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"cyclic AMP") -> r(HGNC:AREG)
label: kin(p(PFH:"PRKA Family")) -> (a(SCHEM:"cyclic AMP") -> r(HGNC:AREG))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284208

6
value: Furthermore, the induction of AR mRNA by cAMP was strongly suppressed by a protein kinase A type I-selective inhibitor, whereas treatment with an exchange protein directly activated by cAMP-specific agonist did not increase AR levels.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284208

RAK-fez5fqMN mRzpD2rZaFcIN1fv0OFzmAGt-jR7c1tY
has assertion: a(SCHEM:Dinoprostone) -> r(HGNC:AREG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.199+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Dinoprostone) -> r(HGNC:AREG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284208

3
value: Similar effects of AR mRNA induction were seen in T cells treated with cAMP-elevating agents such as prostaglandin E(2) and forskolin as well as with the phosphodiesterase inhibitors rolipram and isobutylmethylxanthine.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284208

RAK-VS5dln-Y2jLwFLLeBa5TieGgR5YqSCYK7zaPoY4AE
has assertion: cat(p(HGNC:AKR1B1)) -| a(SCHEM:"Adenosine triphosphate")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.202+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AKR1B1)) -| a(SCHEM:"Adenosine triphosphate")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284219

4
value: Furthermore, ATP content was higher in WT mice compared with ARTg mice during ischemia and reperfusion.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284219

RAOst9UCFJox0X vBVroB2IP-iWUFwUVLw5tCGF2n4cu0
has assertion: path(MESHD:Ischemia) -> path(SDIS:"tissue damage")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.204+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> path(SDIS:"tissue damage")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284219

2
value: Infarct size measured by staining techniques and myocardial damage evaluated histologically were also significantly worse in ARTg
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284219

RAKPaP5-AIx284qoOaN0UoDqjw0FJZE-n1UOvwXoPqgY8
has assertion: path(MESHD:Ischemia) -> sec(p(HGNC:CKM))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.205+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> sec(p(HGNC:CKM))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284219

4
value: Recently, we demonstrated that aldose reductase is a component of myocardial ischemic injury CK release was significantly greater in ARTg mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284219

RAEwuTFkh79t9PZvHTPGRLiO-p4IN3tbbtTXlJaxScbMI
has assertion: kin(p(MGI:Jak2)) -> tscript(p(MGI:Stat1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Jak2)) -> tscript(p(MGI:Stat1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284232

6
value: In response to IFNgamma, SRC-family kinases are required to activate STAT3 (but not STAT1) through tyrosine phosphorylation, whereas the receptor-bound kinases JAK1 and JAK2 are required to activate both STATs.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284232

RAFGVvgEbCskQTSOcW5XkcGcbOejkV8J iUp5xW19E uY
has assertion: bp(GO:"hyperosmotic response") -| r(RGD:Slc4a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.216+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"hyperosmotic response") -| r(RGD:Slc4a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284286

3
value: Toward this end, the expression and regulation of AE1 and SLC26A7 was examined in water deprivation, a condition known to increase the osmolality of the medulla. Rats were subjected to 3 d of water deprivation while having free access to food. Northern hybridizations demonstrated that in the outer medulla, the mRNA expression of SLC26A7 increased by approximately 300% (P < 0.01 versus control; n = 3), whereas the expression of AE1 decreased by approximately 50% (P < 0.05 versus control, n = 3) in water-deprived rats
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284286

RAHO3ASY A6-0SsUzwHI8AZP1KRLE aVZ 428LKYaimhI
has assertion: bp(GO:"response to osmotic stress") -| r(RGD:Slc4a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.218+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to osmotic stress") -| r(RGD:Slc4a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15284286

3
value: Toward this end, the expression and regulation of AE1 and SLC26A7 was examined in water deprivation, a condition known to increase the osmolality of the medulla. Rats were subjected to 3 d of water deprivation while having free access to food. Northern hybridizations demonstrated that in the outer medulla, the mRNA expression of SLC26A7 increased by approximately 300% (P < 0.01 versus control; n = 3), whereas the expression of AE1 decreased by approximately 50% (P < 0.05 versus control, n = 3) in water-deprived rats
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15284286

RAFqKEJg8B0M4VGyrX8L5Otbox7BZ7FeO8v7 z2GcI18E
has assertion: a(CHEBI:staurosporine) -> bp(GO:"chromosome condensation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.229+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:staurosporine) -> bp(GO:"chromosome condensation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15286713

2
value: Non-small-cell lung carcinomas (NSCLCs) are resistant to the induction of apoptosis by conventional anticancer treatment. However, NSCLC cell lines are sensitive to the action of the broad protein kinase inhibitor, staurosporine (STS). In the NSCLC cell line U1810, STS induced the mitochondrial release of apoptosis-inducing factor (AIF) and cytochrome c (Cyt c) followed by activation of caspases, nuclear condensation, DNA fragmentation and finally cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15286713

RAGfEb-ZDGzlNNA3gkTFst104z-1P3yOXv1fDi-5FzA7E
has assertion: p(HGNC:TP53) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.230+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/15286739

3
value: AKT promotes the nuclear translocation of MDM2, thereby negatively regulating p53-mediated apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15286739

RAGrI6sHpPAQ2JkxkddbQhYTPwGyktw6ILurXfXCDNXdg
has assertion: p(HGNC:BCL2) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.242+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BCL2) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15286739

3
value: anti-apoptotic gene BCL2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15286739

RAJvJpuTSd0G2aVsABV6RDBYdYT2VjBkP5RfjFaFxJw00
has assertion: kin(p(HGNC:ATM)) => p(HGNC:BRCA1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.249+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ATM)) => p(HGNC:BRCA1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15286739

5
value: histone H2AX, 53BP1, BRCA1 and NBS1 are all targets of ATM and ATR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15286739

RAKANkm7RwpL5OA 66gMy7SRXy2k4jmw67W47ZCLuh9so
has assertion: p(HGNC:FOXP1) -| r(HGNC:CSF1R)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.260+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FOXP1) -| r(HGNC:CSF1R)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15286807

4
value: Overexpression of MFH/Foxp1 markedly attenuated phorbol ester-induced expression of c-fms, which encodes the M-CSF receptor and is obligatory for macrophage differentiation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15286807

RAHu6C3DVOk7A82zGP2z8IjJMUSHhvuULVfAndPiEsy0k
has assertion: a(CHEBI:"nitric oxide") -> r(HGNC:ACO2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.262+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"nitric oxide") -> r(HGNC:ACO2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15287097

3
value: RESULTS: SNP upregulated mACON enzymatic activity and gene expression in PC-3 cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15287097

RAEJrVY5xDLHU8gaEYAIKhRwo-L06X0FgJP-GwK9IVkOA
has assertion: a(CHEBI:"ascorbic acid") -| r(HGNC:ACO2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.265+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"ascorbic acid") -| r(HGNC:ACO2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15287097

3
value: The addition of ascorbic acid to the SNP treatment resulted in a decrease in mACON enzymatic activity and gene expression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15287097

RAFj-cilL9susVZ2BXvfLT1Sam4b3BjEK6x3RtU3-4i2U
has assertion: kin(p(HGNC:EGFR)) -> path(SDIS:metastasis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.266+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> path(SDIS:metastasis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15288768

4
value: An interaction between EGFR and AR has been demonstrated by immunoconfocal and co-immunoprecipitation analysis in PC3-AR cells, suggesting a possible interference of AR on EGFR signalling by interaction of the two proteins.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15288768

RAIvFRCpCNdVc5CLCo-ARPdAx 9s5W2JXKahcmmIKMics
has assertion: kin(p(HGNC:EGFR)) -> path(SDIS:"tumor cell invasion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.267+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:EGFR)) -> path(SDIS:"tumor cell invasion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15288768

4
value: An interaction between EGFR and AR has been demonstrated by immunoconfocal and co-immunoprecipitation analysis in PC3-AR cells, suggesting a possible interference of AR on EGFR signalling by interaction of the two proteins.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15288768

RAM5JHTwLx4a7DsNSOE7iD4i8sdQfv9zp5izYAaCcNU14
has assertion: p(HGNC:EGF) -> p(HGNC:EGFR,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.269+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGF) -> p(HGNC:EGFR,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15288768

4
value: Immunoprecipitation studies demonstrated a reduction of EGF-induced tyrosine phosphorylation of EGFR in PC3-AR cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15288768

RAFX52Fjx6hadlfT2PYVi1t5mTqrWozVwX4lZA1cDYzFo
has assertion: p(HGNC:AR) -| (p(HGNC:EGF) -> path(SDIS:metastasis))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.272+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AR) -| (p(HGNC:EGF) -> path(SDIS:metastasis))
label: p(HGNC:EGF) -> path(SDIS:metastasis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15288768

5
value: In addition, EGF-stimulated PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15288768

RAHBMiwr36q1Ed-yxzGaED-a420OWl0qi6JfvWEIw1Cgo
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> path(SDIS:metastasis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.275+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)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15288768

3
value: In addition, EGF-stimulated PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15288768

RAPJIWHUsWXfPcSePPWGzR3T5eZNHvPpWUjJpm9D9hYRs
has assertion: p(MGI:Igf1) -> path(SDIS:immortalization)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.283+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Igf1) -> path(SDIS:immortalization)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15291751

3
value: Elevated levels of IGF-I in the circulation are associated with increased risk for the development of prostate cancer in men, and transgenic expression of human IGF-I in mouse epithelial prostate cells results in spontaneous prostate tumorigenesis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15291751

RAFafUBvw9Dyu-1hr9H3LyIlPsxNbOa-l5OKubCu2PMbY
has assertion: p(MGI:Il6) -> tscript(p(MGI:Stat3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.293+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Il6) -> tscript(p(MGI:Stat3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292206

5
value: Stat3 controls cell death and tissue remodeling in the mouse mammary gland during involution, which is partially induced by IL6 and LIF.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292206

RAHjLjUz4T7NtnA0gj5cMzLn BvJ-3HKf4ZYFFscpXZUY
has assertion: cat(p(MGI:Il6st)) -| tscript(p(PFM:"Stat5 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.296+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Il6st)) -| tscript(p(PFM:"Stat5 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292206

6
value: The decline of phosphorylated Stat5 was delayed in gp130-null tissue as compared with wild-type tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292206

RANDJGMj1vKeJWpQPGKuyciZlPPWfQlTs4M5g LS2aCGU
has assertion: p(MGI:Egfr,pmod(P)) => kin(p(MGI:Egfr))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.301+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Egfr,pmod(P)) => kin(p(MGI:Egfr))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292206

5
value: gp130 can transduce signals upon IL6 stimulation, which result in EGFR phosphorylation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292206

RALcabgRS0I2BpNkkVCGmOwslALgGa8Yw1GVCe9WwNu-g
has assertion: kin(p(HGNC:MAP2K7)) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.304+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP2K7)) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292225

6
value: A similar inhibition of activation of the MMTV promoter-driven luciferase construct was seen in HeLa cells transfected with MKK7(D), a constitutively functional activator of JNK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292225

RAOte-6uQmFXpiHUFbNyfEJHLdtKolu6hK9qk1gEBVC2M
has assertion: kin(p(HGNC:MAPK8)) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.308+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK8)) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292225

6
value: The mitogen-activated protein (MAP) kinases, p38 and c-Jun N-terminal kinase (JNK), are important mediators of target gene activation by TNF, and JNK activation was earlier shown to inhibit GR-mediated transcriptional activation by direct phosphorylation of GR at Ser-246.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292225

RAJfPokNqJGS9LH4YK6kfz t-S2jar5XVdtvALP6NrxlE
has assertion: kin(p(HGNC:MAPK9)) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.310+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK9)) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292225

6
value: The mitogen-activated protein (MAP) kinases, p38 and c-Jun N-terminal kinase (JNK), are important mediators of target gene activation by TNF, and JNK activation was earlier shown to inhibit GR-mediated transcriptional activation by direct phosphorylation of GR at Ser-246.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292225

RAL8QH9HUDInFzdNcfqZiIGzFWZb-SULHJs9BOo Zlx4k
has assertion: kin(p(HGNC:MAP2K6)) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.311+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP2K6)) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292225

6
value: Transfection of HeLa cells with MKK6b(E), a constitutively active specific upstream activator of p38, led to a potent inhibition of GR activation of the MMTV promoter-driven luciferase construct.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292225

RAJF97ArWSovlktrntgGFvrGMO4Iey8Jc-ctZ3I2vw768
has assertion: p(MGI:Ctnnb1) -> bp(GO:"cell adhesion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.315+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Ctnnb1) -> bp(GO:"cell adhesion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292239

3
value: These defects in cell adhesion and tissue organization are explained by loss of E-cadherin and beta-catenin localization to cell adhesion sites in both cell culture and in the intact embryos.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292239

RAGqrhIiJkBKhQQQ2GjklYzlpyKyYl122BrPgugs5PDas
has assertion: a(SCHEM:"Tetradecanoylphorbol acetate") -> r(HGNC:NR0B2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.316+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Tetradecanoylphorbol acetate") -> r(HGNC:NR0B2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292277

3
value: Here, we show that SHP expression increases during monocytic differentiaton with exposure HL-60 leukemia cells to a 12-O-tetradecanoylphorbol-13-acetate (TPA) response element, whose treatment induced the SHP promoter activity dependent on c-Jun expression,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292277

RAIA7jWbRNwQ M390Okey42K2WatYEinc2uyXCeE6Pz0c
has assertion: kin(p(HGNC:GSK3B)) -| gtp(complex(NCH:"EIF2B Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.319+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:GSK3B)) -| gtp(complex(NCH:"EIF2B Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: EIF2B is activated through Akt-mediated phosphorylation and inactivation of GSK3B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAPXa6Lu5meu5sLbcfUp-3F35XTKZWJ6cnO1HFBkOgb1A
has assertion: bp(GO:"satellite cell activation") -> r(HGNC:MYF6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.328+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"satellite cell activation") -> r(HGNC:MYF6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

3
value: after proliferation, satellite cells initiate expression of the genes encoding myogenin, mrf4, p21, and, after a permanent exit from the cell cycle, they fuse with damaged myofibers or give rise to new myofibers
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAOGo64TX5UTYWnX j4BFCZ5Sgil5fhPCh6NXqEaQ1ceo
has assertion: p(HGNC:IL4) -> bp(GO:"myoblast fusion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.332+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL4) -> bp(GO:"myoblast fusion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

3
value: by promoting fusion of myoblasts with preformed myotubes, IL4 may actively participate in the regeneration process
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RALrmmRGWy -yYITRF6XO3i9iSl2LTfT-H-nKXL86JL7U
has assertion: p(HGNC:FST) -| complex(p(HGNC:MSTN),p(HGNC:ACVR2B))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.337+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FST) -| complex(p(HGNC:MSTN),p(HGNC:ACVR2B))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

6
value: follistatin can block the binding of myostatin to the activin IIB receptor by interacting with the C-terminal region of a myostatin dimer
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAPkd1H0pmLlHjuqVYM96UrzHudMW4Uw4C1TEsZtDO9S8
has assertion: cat(p(PFH:"HDAC Family")) -| r(HGNC:FST)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.338+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(PFH:"HDAC Family")) -| r(HGNC:FST)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: follistatin gene expression is activated by exposure of skeletal muscle cells to deacetylase inhibitors
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RANQXoCQNzRu6m5Pzdko2MJzmgBVdjoiZt5mQskCPmNq8
has assertion: bp(MESHPP:Exercise) -> bp(GO:"satellite cell activation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.342+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Exercise) -> bp(GO:"satellite cell activation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

2
value: microtraumas resulting from chronic exercise also lead to satellite cell activation and proliferation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAFvjdLaQr2OAj8fhw27EesdrS8WlscCXmTWpLJiTfn98
has assertion: kin(p(HGNC:AKT1)) => p(EGID:2475,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.345+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) => p(EGID:2475,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: once Akt1 is activated, it initiates a cascade of phosphorylation events targeting mammalian target of rapamycin, mTOR, which in turn phosphorylates the p70S6 kinase and GSK3B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAKgxrgmh6e9aHldcJ9TzhgqiNqjkgWoEjb-zrqXyuFWU
has assertion: kin(p(HGNC:AKT1)) => p(HGNC:GSK3B,pmod(P,S))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.346+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) => p(HGNC:GSK3B,pmod(P,S))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: once Akt1 is activated, it initiates a cascade of phosphorylation events targeting mammalian target of rapamycin, mTOR, which in turn phosphorylates the p70S6 kinase and GSK3B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAKRqBuHo1xe 1QreBoOTdtLLb7IPnNm8HMlW RDQuVCE
has assertion: kin(p(HGNC:AKT1)) -> kin(p(EGID:2475))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.348+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) -> kin(p(EGID:2475))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

6
value: once Akt1 is activated, it initiates a cascade of phosphorylation events targeting mammalian target of rapamycin, mTOR, which in turn phosphorylates the p70S6 kinase and GSK3B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAL-d1m F8e7tYQukdtKPkDh5Nn8sDNX4oC6dEHGuizJk
has assertion: kin(p(EGID:2475)) -> p(HGNC:RPS6KB1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.349+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(EGID:2475)) -> p(HGNC:RPS6KB1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: once Akt1 is activated, it initiates a cascade of phosphorylation events targeting mammalian target of rapamycin, mTOR, which in turn phosphorylates the p70S6 kinase and GSK3B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAI8s8cB1ydPfsXnOiPYeqynZeO2I- sE29L7at Y9vw4
has assertion: bp(GO:"satellite cell activation") -> r(HGNC:MYF5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.351+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"satellite cell activation") -> r(HGNC:MYF5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

3
value: once satellite cells are activated, they express the genes encoding the 2 myogenic regulatory factors Myf5 and MyoD, which are not detectable in quiescent cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAPtM0Q9i-sIH3mIBipPiOuhpJ0hWscJn5-Ru4iyrYzt8
has assertion: bp(GO:"satellite cell activation") -> r(HGNC:MYOD1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.352+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"satellite cell activation") -> r(HGNC:MYOD1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

3
value: once satellite cells are activated, they express the genes encoding the 2 myogenic regulatory factors Myf5 and MyoD, which are not detectable in quiescent cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAEm4EzJuhkDgW9vomadyRJCGrf7pCIflkvAKMSaJgK E
has assertion: p(HGNC:IRS1) -> gtp(p(HGNC:HRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.353+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IRS1) -> gtp(p(HGNC:HRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: phosphorylated IRS1 also stimulates the Ras-Raf-MEK-ERK pathway, a MAPK pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAO4CSFBK7A8zB6sr0KeD2c1fTerbCTcVphFKW5M w g8
has assertion: kin(p(EGID:2475)) -| p(HGNC:EIF4EBP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.354+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(EGID:2475)) -| p(HGNC:EIF4EBP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: phosphorylation of mTOR represses, through an adaptor protein known as Raptor, 4EBP1, an inhibitor of EIF4E
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAJnBHVi9dscshpXbMZ8F6jcYpBHOgT-vCZyBIwwzpVm0
has assertion: kin(p(HGNC:IGF1R)) => p(HGNC:IRS1,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.365+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:IGF1R)) => p(HGNC:IRS1,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15292521

5
value: upon binding of IGF1, the IGFR, which is a receptor tyrosine kinase, becomes phosphorylated and recruits the substrate IRS1, leading to the activation of the lipid kinase PI3K
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15292521

RAPjPuqgbRNf-SVREYbxshdZpGLSofWk l 03OsjVHqqk
has assertion: kin(p(HGNC:RPS6KA2)) -> tscript(p(HGNC:CREB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.370+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RPS6KA2)) -> tscript(p(HGNC:CREB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

6
value: Activated p90rsk phosphorylates several transcription factors including Elk and the cAMP-response element-binding protein (CREB) and the activating protein 1 family of c-Jun, c-fos and activating transcription factor (Pearson et al. 2001).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAKw9m4el2SyRQtTMspGXlK18SOfr4HVwQcMlvt9qyRyA
has assertion: kin(p(HGNC:RPS6KA2)) -> tscript(p(HGNC:JUN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.373+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RPS6KA2)) -> tscript(p(HGNC:JUN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

6
value: Activated p90rsk phosphorylates several transcription factors including Elk and the cAMP-response element-binding protein (CREB) and the activating protein 1 family of c-Jun, c-fos and activating transcription factor (Pearson et al. 2001).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RANnAMVshnLdMYFlLTR0fEp U2V0CTHrAWJQTx8XkCslc
has assertion: bp(GO:"muscle contraction") -> r(HGNC:FOS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.375+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"muscle contraction") -> r(HGNC:FOS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

3
value: Activation of JNK in response to skeletal muscle contraction is associated with a rapid induction of the early response genes c-Jun and c-fos, as evidenced by increased mRNA levels (Aronson et al. 1997a).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAPITH9xBdcPG9cpMXIwBGMzCLoJghI1w5cxdpzw 6cI0
has assertion: bp(MESHPP:Exercise) -> r(HGNC:DMD)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.377+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Exercise) -> r(HGNC:DMD)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

3
value: Examples of genes having MEF2-binding sites include GLUT4, creatine kinase, AMP deaminase, myoglobin, myosin (heavy light chains), dystrophin, MyoD and cJun (Black Olson, 1998).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAHckNscYUbIxLbkSqF6gBBE9rHtZXlG9dG 0-Ko hqn8
has assertion: bp(MESHPP:Exercise) -> r(HGNC:JUN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.379+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Exercise) -> r(HGNC:JUN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

3
value: Examples of genes having MEF2-binding sites include GLUT4, creatine kinase, AMP deaminase, myoglobin, myosin (heavy light chains), dystrophin, MyoD and cJun (Black Olson, 1998).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RANrpvmU3MqkCQ7NG5-bORjUIEcit8WSnhuX 3XdZtlKU
has assertion: bp(MESHPP:Exercise) -> r(HGNC:MYL3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.384+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Exercise) -> r(HGNC:MYL3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

3
value: Examples of genes having MEF2-binding sites include GLUT4, creatine kinase, AMP deaminase, myoglobin, myosin (heavy light chains), dystrophin, MyoD and cJun (Black Olson, 1998).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAMarMxB0PvI6bPmDDY 7h8dIv6aVWTqG6qwIpe9vMqBg
has assertion: bp(MESHPP:Exercise) -> r(HGNC:SLC2A4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.390+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Exercise) -> r(HGNC:SLC2A4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

3
value: Examples of genes having MEF2-binding sites include GLUT4, creatine kinase, AMP deaminase, myoglobin, myosin (heavy light chains), dystrophin, MyoD and cJun (Black Olson, 1998).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAPyvdGnZ2czqrz9Z0tUKOIaJHgNH 2oaqCiXnVH7CgDY
has assertion: tscript(p(PFH:"MEF2 Family")) -> r(HGNC:MYH9)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.396+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(PFH:"MEF2 Family")) -> r(HGNC:MYH9)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

5
value: Examples of genes having MEF2-binding sites include GLUT4, creatine kinase, AMP deaminase, myoglobin, myosin (heavy light chains), dystrophin, MyoD and cJun (Black Olson, 1998).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAIhpTW3JOnSq82W-mTAg-82OIqsv2IK2Vabax-b3n-M0
has assertion: a(SCHEM:"SB-203580") -| kin(p(RGD:Mapk14))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.415+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"SB-203580") -| kin(p(RGD:Mapk14))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

4
value: PD98059 (MAPK/ERK1 inhibitor) and SB203580 (p38 MAPK inhibitor) respectively. In isolated rat skeletal muscle specific inhibition of ERK1/2 by PD98059 completely abolishes contraction-mediated p90rsk activity (Ryder et al. 2000).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAPnrXa4EtKLtNp6pCOwdqDMyuf1G4EbmtXLmi8o0Fjmc
has assertion: kin(p(HGNC:MAP3K7)) -> kin(p(HGNC:MAP2K6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.425+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K7)) -> kin(p(HGNC:MAP2K6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294035

6
value: exercise leads to the activation of at least three MAPK signalling pathways, i.e. ERK1/2, p38 MAPK and JNK, in skeletal muscle (Zierath, 2002).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294035

RAHPzxOWGAIIPAGGeNm1ULXGi1wl2VKUoHrXkiuUyFObs
has assertion: tscript(p(HGNC:PPARGC1A)) -> tscript(complex(NCH:"AP-1 Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.474+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:PPARGC1A)) -> tscript(complex(NCH:"AP-1 Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294043

5
value: Activation of NRF-1 by PGC-1 increases the expression of genes that encode mitochondrial respiratory chain proteins (Scarpulla, 2002) and 5-aminolevulinate synthase (Briadotti et al. 1993), as well as mitochondrial transcription factor A, a regulator of mitochondrial DNA transcription and replication
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294043

RAKiEdAr xplW6shkiNDWu3G1irV7gAjpVPG1kHWDc94Y
has assertion: tscript(p(HGNC:PPARGC1A)) -> tscript(p(HGNC:NRF1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.476+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:PPARGC1A)) -> tscript(p(HGNC:NRF1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294043

6
value: Activation of NRF-1 by PGC-1 increases the expression of genes that encode mitochondrial respiratory chain proteins (Scarpulla, 2002) and 5-aminolevulinate synthase (Briadotti et al. 1993), as well as mitochondrial transcription factor A, a regulator of mitochondrial DNA transcription and replication
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294043

RAP Y0RmAfL1J0kJJcMvBwwW zilFeahAqoWJ1PcO iIk
has assertion: kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,863))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.480+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,863))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294048

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294048

RAFaOCchA-VAQxo67Przv33RlpqxVHwNakVap4-LCNfUs
has assertion: kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,959))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.482+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,959))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294048

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294048

RALtrpQ6LlxfztM38ohvBcs8DFCJiV7EFaAeMcQF d8LY
has assertion: kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,960))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.483+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Prka Family")) => p(RGD:Lipe,pmod(P,S,960))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294048

5
value: PhosphoElm data from PMID 15212693
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294048

RAJrl2DRbfLftXv30 1-FvV977-UWODEo-yBZC 7ADNGU
has assertion: a(SCHEM:"serum insulin") -> (bp(MESHPP:Exercise) -> bp(GO:"skeletal muscle hypertrophy"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.511+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum insulin") -> (bp(MESHPP:Exercise) -> bp(GO:"skeletal muscle hypertrophy"))
label: bp(MESHPP:Exercise) -> bp(GO:"skeletal muscle hypertrophy")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294054

3
value: Indeed, each of these select proteins is indispensable in mediating skeletal muscle growth and, whereas proposing the up-regulation of distinct proteins as potential markers of hypertrophy is tempting, a coordinated response from multiple signal transduction pathways is essential to the overall process. Integration of signalling by insulin, amino acids and resistance exercise A thorough review of amino acids and insulin and their contribution to regulating skeletal muscle protein synthesis is beyond the scope of the present paper. Thus, the intent of the present brief overview will be to focus exclusively on the impact of amino acids or insulin on protein synthesis in the context of resistance exercise. Without question, investigating the singular role of amino acids or insulin in promoting changes in skeletal muscle protein synthesis with resistance exercise is crucial to elucidating mechanisms regulating muscle hypertrophy. However, in a physiological state the concept is essentially irrelevant, as insulin and amino acids do not function in isolation because both participate to optimize the anabolic response in skeletal muscle. Nonetheless, key findings in both areas will be briefly highlighted to emphasize their contribution with resistance exercise. Although insulin concentrations remain relatively unchanged in the recovery period following resistance exercise (Kraemer et al. 1998; Biolo et al. 1999; Hernandez et al. 2000), a permissive amount of insulin is required to mediate increases in skeletal-muscle protein synthesis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294054

RAE-uFJC9wIxT2IgzsQl5OvR-zYb0U6o24clAgXHSheo0
has assertion: path(SDIS:denervation) -> r(MGI:Qdpr)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.538+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:denervation) -> r(MGI:Qdpr)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294855

3
value: After 14-day simultaneous denervation of the soleus (Sol), tibialis anterior (TA), extensor digitorum longus (EDL), and gastrocnemius (Gastr) muscles by sciatic nerve section, DHPR mRNA increased preferentially in the Sol and TA (+1.6-fold), whereas it increased in the EDL (+1.6-fold) and TA (+1.8-fold) after selective denervation of these muscles by peroneal nerve section
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294855

RANN4Hxi8WKjrznG j72rExdkT84BspKdp3vf6HMLDTik
has assertion: p(HGNC:KRAS,sub(G,13,D)) => gtp(p(HGNC:KRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.542+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

1
has substitution: G,13,D
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(G,13,D)) => gtp(p(HGNC:KRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294875

5
value: From mutations file
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294875

RAMPLtcTd42H5bZImcWaEWyW7439w9teZFHPpNR1DeYNc
has assertion: kin(p(HGNC:FLT1)) -> p(HGNC:FLT1,pmod(P,Y))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.546+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:FLT1)) -> p(HGNC:FLT1,pmod(P,Y))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294883

5
value: Flt1 reveals a weak tyrosine autophosphorylation in response to VEGF
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294883

RAL 6z7kAlqLvE8Qjf-FqRJF8IcPnWqz2f3Nuc-1dveEc
has assertion: kin(p(HGNC:TGFBR1)) -> kin(p(HGNC:MAP2K2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.552+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:TGFBR1)) -> kin(p(HGNC:MAP2K2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15294900

6
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15294900

RAICkTcqXV0lTq9UXy-Jwq434ZbagRwRMfIW7qtZPOid0
has assertion: complex(p(HGNC:TNF),p(HGNC:TNFRSF1A)) => cat(p(HGNC:TNFRSF1A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.593+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:TNF),p(HGNC:TNFRSF1A)) => cat(p(HGNC:TNFRSF1A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15300201

7
value: Overexpression of NCOA-1, NCOA-2, and NCOA-3 enhanced E2-mediated gene expression by 3.17 +/- 0.51-, 2.33 +/- 0.8-, and 3.65 +/- 0.65-fold, respectively, and enhanced cell survival by suppressing tumor necrosis factor alpha (TNF-alpha)-induced cell death Overexpression of NCOA-1 and NCOA-3 exerted potent survival effects in breast carcinoma cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15300201

RAIQJBsA-XVGqG69s6tt9G-N thO4ttM6RT8JjL9yXLYU
has assertion: p(HGNC:BIRC6) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.608+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BIRC6) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15300255

3
value: Apollon inhibits apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15300255

RAOdIu5x9KyAV8A h6b7VwjuJMIsmn dqTwKU1NVfgNVk
has assertion: path(SDIS:"food intake") -> r(MGI:Car3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.619+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(MGI:Car3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302862

3
value: Supplementary Table 1. Gene Regulation by Caloric Restriction and Compounds Including Nuclear Receptor Agonists downregulated by caloric restriction
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302862

RAG3Rmq3QwmRn1AbvDF9EKbUep94Cl6ekMr-rx3G1ejfM
has assertion: path(SDIS:"food intake") -> r(MGI:Ethe1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.625+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(MGI:Ethe1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302862

3
value: Supplementary Table 1. Gene Regulation by Caloric Restriction and Compounds Including Nuclear Receptor Agonists downregulated by caloric restriction
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302862

RANF30kMywGNDOAYecKo8JAOxkrH1q2PAe8ANdOjxglS4
has assertion: path(SDIS:"food intake") -> r(EGID:109901)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.627+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(EGID:109901)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302862

3
value: Supplementary Table 1. Gene Regulation by Caloric Restriction and Compounds Including Nuclear Receptor Agonists downregulated by caloric restriction
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302862

RANCIJ6Xj1IJtnIcrUeizuCeHtDfejEUVvS9ztqbTL3MY
has assertion: path(SDIS:"food intake") -> r(MGI:Tmem147)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.645+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -> r(MGI:Tmem147)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302862

3
value: Supplementary Table 1. Gene Regulation by Caloric Restriction and Compounds Including Nuclear Receptor Agonists downregulated by caloric restriction
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302862

RAMCHWudAPJARzUkEjsLn2Emcr4PBTMuWCRUdpu43lJqg
has assertion: p(HGNC:JAZF1) -| tscript(p(HGNC:NR2C2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.663+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:JAZF1) -| tscript(p(HGNC:NR2C2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302918

5
value: Yeast two-hybrid analysis using the ligand-binding domain (LBD) of TAK1 as bait identified a novel TAK1-interacting protein, referred to as TIP27, which functions as a repressor of TAK1-mediated transactivation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302918

RAHa6PN181tC 2dhHkn2HNb7DurZ8f9vFRs4RpCaqHmkk
has assertion: p(HGNC:EGR3) -> bp(GO:"spindle assembly")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.666+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EGR3) -> bp(GO:"spindle assembly")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302938

3
value: Egr3 expression is required for the formation of muscle spindle fibers
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302938

RAMLeBnIOOSoQz OCZKQdM 9NcsIKViQ7SprkD8Gwqxzk
has assertion: p(HGNC:NRG1) -> surf(p(PFH:"CHRM Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.668+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NRG1) -> surf(p(PFH:"CHRM Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15302938

5
value: in addition to increasing the expression of acetylcholine receptors on the myotube surface, NRG treatment results in a transient increase of several members of the early growth response (Egr) family of transcription factors. Three Egrs, Egr1, -2, and -3, are induced within the first hour of NRG treatment, with Egr1 and -3 RNA levels showing the most significant increases of approximately 9- and 16-fold, respectively
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15302938

RANOvGs2QHtH6sCgZF5vGJC1yicNRru8sg6GipaNqtBCs
has assertion: a(SCHEM:"serum glucose") -> p(HGNC:ICAM1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.673+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum glucose") -> p(HGNC:ICAM1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304054

3
value: \"Intermittent high glucose enhances ICAM-1, VCAM-1, E-selectin and interleukin-6 expression in human umbilical endothelial cells in culture: the role of poly(ADP-ribose) polymerase.\" We found that oscillating glucose was more effective in triggering the generation of nitrotyrosine and inducing the expression of adhesion molecules and IL-6 than stable high glucose.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304054

RAGPems3bIU8fpks7bW-MuKLYTJjWIaZfl PSSqgIdlaQ
has assertion: bp(GO:"response to UV") -> (cat(p(HGNC:CASP3)) -> kin(p(HGNC:PRKCD)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.693+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to UV") -> (cat(p(HGNC:CASP3)) -> kin(p(HGNC:PRKCD)))
label: cat(p(HGNC:CASP3)) -> kin(p(HGNC:PRKCD))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304079

7
value: The constitutively active catalytic domain of protein kinase C (PKC)delta is an apoptotic effector generated by caspase-3 cleavage of full-length PKCdelta in response to a wide variety of apoptotic stimuli, including UV radiation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304079

RAKUIf3PJ-PNODITKSEDb7jOCk-aCW0N4CTJ TEpee1zI
has assertion: a(CHEBI:etoposide) -> p(HGNC:H2AFX,pmod(P,S,140))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.710+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:etoposide) -> p(HGNC:H2AFX,pmod(P,S,140))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304327

3
value: In KD clones, but not in RD-clones, formation of etoposide-induced gamma-H2AX was increased, indicating that PrxV inhibits conversion of topoisomerase II cleavage complexes into double-strand DNA breaks but this inhibition is not caused by its antioxidant activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304327

RAL16YIFAXcQLNzJ1oVq70AyfP6fRxcdYsudlK8cwIGlE
has assertion: phos(p(HGNC:PTEN)) -| tscript(p(HGNC:RUNX2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.722+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTEN)) -| tscript(p(HGNC:RUNX2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304489

6
value: Although transfection resulted in the inhibition of RUNX2 activity, PTEN wild type was more effective at inhibiting RUNX2 DNA binding (70% inhibition) than the mutant vector (30% inhibition) (Fig. 3D).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304489

RAPAmhdRQP7BCsavkHPP7JnSjt-vdJIRuQC SqJbaZeqk
has assertion: p(HGNC:IGF1) -> kin(p(HGNC:MAPK3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IGF1) -> kin(p(HGNC:MAPK3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304489

5
value: IGF-1 increased active ERK1/2 within 5 min, a response that was ablated by pretreatment with LY294002.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304489

RALsbhKVWrhvJbdcmypSy Wt7ADWk-nSL2My25XcDv54
has assertion: p(HGNC:IGF1) -> tscript(p(HGNC:RUNX2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.728+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IGF1) -> tscript(p(HGNC:RUNX2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15304489

5
value: IGF-1 treatment increased RUNX2 DNA binding activity in HBME cells up to 10-fold relative to untreated cells (Fig. 2A).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15304489

RAOcqfsNPYJtw1vW8-NcPFk-U8oWx1kfXehFu9-35Y2IA
has assertion: p(HGNC:HELLS) -| path(MESHD:Neoplasms)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.742+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:HELLS) -| path(MESHD:Neoplasms)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15305370

3
value: loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading lung cells to malignancy or its progression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15305370

RAIA5G 1ZEBgE3nUuKfwbuiSo1XJ INrs-bqjuKNd7t4I
has assertion: path(MESHD:Ischemia) -> r(RGD:Nfib)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.755+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(RGD:Nfib)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15306117

3
value: Most robustly expressed were gene sequences NFI-B, ATP1B1, RHOGAP, PLA2G4A, BAX, CASP3, P53, MAO-A, FRA1, HSP70.2, and NR4A1 (NUR77) These data indicate that ischemia elicits expression of an array of functional gene clusters
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15306117

RAGNUvGLbW qjGZ8AUnbCRye5Y39CBWkRADR8V8sqbDGE
has assertion: tscript(complex(NCH:"AP-1 Complex")) -> r(HGNC:GSTP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.757+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCH:"AP-1 Complex")) -> r(HGNC:GSTP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/1530652

4
value: Both the stimulated expression of GST-P gene by TPA and that by over-expressed c-Jun were suppressed to the basal level by dexamethasone, an inhibitor of AP-1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/1530652

RAOtm5YbxJg5BzqeTURR1Dz3z40Z0FgeOyDZqszZ8mGfU
has assertion: bp(MESHPP:Obesity) positiveCorrelation kin(p(MGI:Rps6kb1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.761+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation kin(p(MGI:Rps6kb1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15306821

4
value: Moreover, wild-type mice on a high fat diet as well as K/K A(y) and ob/ob (also known as Lep/Lep) mice-two genetic models of obesity-have markedly elevated S6K1 activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15306821

RAKpiVvtixHHVACxFfOGRfWKvh8LJijWGpmsG9V56NAXo
has assertion: bp(MESHPP:Apoptosis) -> p(HGNC:PHB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.765+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Apoptosis) -> p(HGNC:PHB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15308007

3
value: identified by MALDI-TOF Up-regulation of TrpRS, RS, prohibitin and down-regulation of BTF3 were involved in inhibition of transcription and protein synthesis in the apoptotic K562 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15308007

RAOYZiGReLKzOCJgLDyw5NISyt7qHoB3vcPYbhmbnYWhM
has assertion: p(HGNC:FOXO3) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.768+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FOXO3) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15308101

3
value: Foxo3a deficiency leads to spontaneous lymphoproliferation, associated with inflammation of several organs, in the absence of overt apoptotic defects.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15308101

RAHGN5DP6N9uAQb-zs3DEd3oaiUo0S-8AqcpBsC2VyoZQ
has assertion: kin(p(HGNC:ACVR1)) -> tscript(p(HGNC:SMAD9))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.788+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ACVR1)) -> tscript(p(HGNC:SMAD9))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15308665

6
value: BMP signaling leading to Smad1/5/8 activation via ALK2/3/6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15308665

RAMSlmLgcoNGRZBmN8WGIdrtShuScbu1gOd0f2oeEtjpA
has assertion: kin(p(HGNC:BMPR1A)) -> tscript(p(HGNC:SMAD9))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.792+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:BMPR1A)) -> tscript(p(HGNC:SMAD9))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15308665

6
value: BMP signaling leading to Smad1/5/8 activation via ALK2/3/6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15308665

RAL8SoF-wpFhdUK-7MLYt0GhX-hRxmHJZP9ju8C1bwcrQ
has assertion: kin(p(HGNC:BMPR1B)) -> tscript(p(HGNC:SMAD5))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.795+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:BMPR1B)) -> tscript(p(HGNC:SMAD5))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15308665

6
value: BMP signaling leading to Smad1/5/8 activation via ALK2/3/6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15308665

RAFSJSxHgKz-YgUBgK0nMoGJRqOGmVvtrku7R1-2S-5Hc
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> bp(GO:"endothelial cell activation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.807+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> bp(GO:"endothelial cell activation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15309203

2
value: Oxidized low density lipoprotein (ox-LDL), a marker of oxidative stress, is present in the plasma as well as in the atherosclerotic arteries of patients with atherosclerosis. Ox-LDL leads to endothelial activation, dysfunction and injury
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15309203

RAMuPQ-SvUFZzVLi4I RAdkCJCxV6OogPHaZjvDqrRPIU
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:NPM1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.815+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:NPM1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15310764

3
value: Here we report that this proliferation-promoting protein is strongly induced in response to hypoxia in human normal and cancer cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15310764

RAI8u8M7g6dIMq1yPkG0TMcD595X-jnZ3iloAQHQ8yriM
has assertion: bp(GO:"response to hypoxia") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.817+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> bp(MESHPP:Apoptosis)
label: p(HGNC:NPM1) -| (bp(GO:"response to hypoxia") -> bp(MESHPP:Apoptosis))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15310764

4
value: Suppression of NPM expression by small interfering RNA targeting NPM increases hypoxia-induced apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15310764

RAItfPVrhUFRUEFYPuHMEPJLwUbmB3qzIYIfKfNcVDkOo
has assertion: p(HGNC:VHL) -| p(HGNC:HIF1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.825+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:VHL) -| p(HGNC:HIF1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15312748

4
value: Exposure of HEL, K562, and Hep-G2 cells to hypoxia for 18 hours resulted in a significant increase in FECH mRNA expression (p Hypoxia also transactivated the minimal promoter for the FECH gene in the cells. Transient co-expression of wild-type HIF-1alpha or a dominant negative HIF-1alpha with the FECH minimal promoter luciferase construct stimulated or blocked FECH promoter activity, respectively. Expression of the von Hippel-Lindau (VHL) tumor suppressor factor blocked the expression of both FECH mRNA and HIF-1alpha protein
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15312748

RAFxkk9WDS6L2tIUcakdv71vAHxh YhHZrQp43d H7MzE
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:FECH)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.826+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:FECH)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15312748

3
value: Exposure of HEL, K562, and Hep-G2 cells to hypoxia for 18 hours resulted in a significant increase in FECH mRNA expression (p Hypoxia also transactivated the minimal promoter for the FECH gene in the cells. Transient co-expression of wild-type HIF-1alpha or a dominant negative HIF-1alpha with the FECH minimal promoter luciferase construct stimulated or blocked FECH promoter activity, respectively. Expression of the von Hippel-Lindau (VHL) tumor suppressor factor blocked the expression of both FECH mRNA and HIF-1alpha protein
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15312748

RAKqMwEL4UhPZKvSgng9iVdI-h6VtPcBZcM7t7Faouv3U
has assertion: a(SCHEM:"Cyclic GMP") -| bp(GO:"platelet aggregation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.830+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Cyclic GMP") -| bp(GO:"platelet aggregation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15312990

2
value: Activation of the NO/cGMP pathway results in a strong reduction of platelet aggregation elicited by agonists such as thrombin (Azuma et al., 1986; Radomski et al., 1987; Benjamin et al., 1991; Moro et al., 1996; Rao et al., 1990).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15312990

RALuiHuXVArN2cdvCH3wFqI3CqpuLDAvHxKg5r05wSCnw
has assertion: a(CHEBI:"nitric oxide") -| r(RGD:Gucy1a3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.831+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"nitric oxide") -| r(RGD:Gucy1a3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15312990

3
value: NO has been described to inhibit sGC expression and sGC activity in a cGMP-dependent manner (Filippov et al., 1997).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15312990

RAIL4UUZ1DKoN3gxwC1f-yN Lew3yNf3avfhJ7FbPixzA
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:ATF3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.847+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:ATF3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAPcGWQkF5RuCru0KHEtQvMCSXSLAuHNhkyqjuT5NbVGs
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:BUD31)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.850+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:BUD31)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAMSf5WsU7Z9tYen2dh4 nHSIDBQ4fY18yKwnWGC6NiHA
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:CRABP2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.854+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:CRABP2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RANH6XH26SDVhCHawqHvga5LHGq5uKCJMScTd3ldA6-i0
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:IGFBP4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.865+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:IGFBP4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAFGSty2YFlFQtIVmf7W1Qx1IiOEQ7sjVKnJ45POXnuMk
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:MAP2K1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.868+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:MAP2K1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RANXTm8ppGuAXpukTAqQZvGa4KIHOoBcWw65jJq5A17k0
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:MEF2A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.869+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:MEF2A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAHookFsAy67u4HekFh5-ckqlr-BjKc-Xo1urFdn8yfmI
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:PDK3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.874+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:PDK3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAHeEKVE9NbnCqgx4d5SJ2cKu52qXZgLEUuz4ZgkeGJsY
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:PRRX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.878+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:PRRX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAG5Un6PG4bMU2C1ighYgekk8c6YPIxHOSetg9FrWjpxU
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:TAX1BP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.887+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:TAX1BP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314157

3
value: TABLE 2. Hypoxia-induced translationally regulated genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314157

RAJRyT9pCuCLI-jGcpnaGsfN9g4GRet 9E4ZybQtkPKPk
has assertion: tscript(p(HGNC:TP53)) -| bp(GO:"cell cycle")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.898+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP53)) -| bp(GO:"cell cycle")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314174

4
value: together to form a ternary complex. We show that, when overexpressed, L23 inhibits HDM2-induced p53 polyubiquitination and degradation and causes a p53-dependent cell cycle arrest.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314174

RAOKBS0ll9qZjV5nQN C615lCedn5vTwRimiYjpT2LD3o
has assertion: tscript(p(HGNC:ETS2)) -> p(HGNC:BCL2L1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.902+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ETS2)) -> p(HGNC:BCL2L1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15314206

5
value: Downregulation of Ets2 in prostate cancer cells was associated with reduced levels of the anti-apoptotic protein bcl-x(L) and growth regulatory factors cyclin D1 and c-myc.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15314206

RAKDfG7pnyyIsUemLRvVDBK2KFyOD4fEQoYx8ZJlmXl5c
has assertion: a(SCHEM:"Tetradecanoylphorbol acetate") -> kin(p(PFH:"PRKC Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.911+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Tetradecanoylphorbol acetate") -> kin(p(PFH:"PRKC Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/1531537

4
value: A cultured myocardial cell model was used to examine the role of protein kinase C-dependent pathways in the transcriptional activation of two cardiac muscle genes [myosin light chain 2 (MLC-2) and atrial natriuretic factor (ANF)] during alpha-adrenergic receptor-mediated hypertrophy. Phorbol ester (phorbol 12-myristate 13-acetate) and the alpha-adrenergic agonist phenylephrine both activate protein kinase C (PKC) and induce 4- to 5-fold increases in the expression of MLC-2 and ANF promoter/luciferase reporter genes with little effect on Rous sarcoma virus/luciferase or minimal prolactin promoter/luciferase genes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/1531537

RAPQhVJ1eY0apRrbeZIpyLxX5MAK5C5N1GSEwKf5HL8jU
has assertion: kin(p(PFH:"PRKC Family")) -> p(EGID:29895)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.916+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"PRKC Family")) -> p(EGID:29895)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/1531537

5
value: A cultured myocardial cell model was used to examine the role of protein kinase C-dependent pathways in the transcriptional activation of two cardiac muscle genes [myosin light chain 2 (MLC-2) and atrial natriuretic factor (ANF)] during alpha-adrenergic receptor-mediated hypertrophy. Phorbol ester (phorbol 12-myristate 13-acetate) and the alpha-adrenergic agonist phenylephrine both activate protein kinase C (PKC) and induce 4- to 5-fold increases in the expression of MLC-2 and ANF promoter/luciferase reporter genes with little effect on Rous sarcoma virus/luciferase or minimal prolactin promoter/luciferase genes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/1531537

RAFxSO8fnjR5ckmIyEEpk5P-DBCBMnSr3Dyl43jPB-ncU
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(RGD:Adm)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.919+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(RGD:Adm)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15315911

3
value: The present study demonstrates for the first time that AM and its receptor component (CRLR/RAMP2) mRNAs were concomitantly expressed in various adipose tissues, whose tissue-specific upregulation was induced during the development of obesity;whereas steady-state AM mRNA levels conversely decreased in other organs, such as kidney and liver
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15315911

RAFNhwQdtS3mzNxDk69S853nsDYcTKAT4YoihZDkq5fDk
has assertion: bp(MESHPP:Obesity) positiveCorrelation r(RGD:Adm)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.921+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:Obesity) positiveCorrelation r(RGD:Adm)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15315911

3
value: The present study demonstrates for the first time that AM and its receptor component (CRLR/RAMP2) mRNAs were concomitantly expressed in various adipose tissues, whose tissue-specific upregulation was induced during the development of obesity;whereas steady-state AM mRNA levels conversely decreased in other organs, such as kidney and liver
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15315911

RAE1MgouPPhlNj1NXHjt0Zb2qRzdrj3vcctItIXRGWkk4
has assertion: bp(GO:aging) -| r(MGI:Smc4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:26.994+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(MGI:Smc4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15317747

3
value: Hook1, Tuba1, Tubd1, Dncic2, Kif3b, Rnf19/Dorfin, Pcnt2, Nin and Smc4l1, all decreased with maternal aging
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15317747

RAJ-igJEdA7wmQCW2PBFRtnQukt8QcAjaONDDkKjMvdMQ
has assertion: tscript(p(PFH:"RAR Family")) -> r(HGNC:NEDD9)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.015+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(PFH:"RAR Family")) -> r(HGNC:NEDD9)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15318809

5
value: We report here the identification of 14 genes that are % rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), % eight of which were previously not known to be atRA responsive (BTBD11, % calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15318809

RAPqRF58J68bisEc771vK9Oz3 26 aBFC1 nBGDUptDj4
has assertion: a(SCHEM:"1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid") -| (cat(p(HGNC:ADRB2)) -> kin(p(HGNC:MAPK3)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.025+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid") -| (cat(p(HGNC:ADRB2)) -> kin(p(HGNC:MAPK3)))
label: cat(p(HGNC:ADRB2)) -> kin(p(HGNC:MAPK3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15319437

7
value: In contrast, chelation of intracellular Ca2+ with BAPTA/AM (20 uM) almost fully blunted ERK1/2 phosphorylation (n = 4; p < 0.002) as well as H-Ras activation (n = 5; p < 0.001) induced by the beta2-AR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15319437

RALrOzyv2aEAtD3lZqIJ0DWGddBEnd789dvZkiRKy 4vI
has assertion: cat(p(HGNC:PLCE1)) -> a(SCHEM:Calcium)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.027+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:PLCE1)) -> a(SCHEM:Calcium)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15319437

4
value: In contrast, expression of lipase-inactive H1144L PLC-epsilon (27), which inhibited PLC and Ca2+ signaling in HEK-293 cells (35), strongly reduced (n = 4; p < 0.001) the adrenaline-induced ERK1/2 phosphorylation and H-Ras activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15319437

RANCN0sI6jqZIV52vaWbqVN6JUGrZ3Vorfe3cmQshdZ9g
has assertion: complex(p(HGNC:INHBA),p(HGNC:INHBA)) -> p(HGNC:GNRH1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.040+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:INHBA),p(HGNC:INHBA)) -> p(HGNC:GNRH1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15319828

6
value: Second, activin up-regulates gonadotropin-releasing hormone receptor (GnRHR) gene expression, leading to alterations in the synthesis and release of both gonadotropins in response to GnRH. Third, activin can stimulate GnRH release from GnRH neurons in the hypothalamus and thereby affect FSH and LH secretion.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15319828

RAK7ZsWGyy9wYXlX-e94RsYQ4yW1lxukxAcxoNos6dXro
has assertion: p(HGNC:CREBBP) => p(PFH:"Histone H4 Family",pmod(A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.046+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CREBBP) => p(PFH:"Histone H4 Family",pmod(A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: 4. CBP/p300 family H3, H4, H2A, H2B; Nonhistone proteins Worm to human Global coactivator
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAFymSnVFGSx6ayLTArCgcBgH1kIoH-2q pT65O4v7x70
has assertion: p(HGNC:ATF2) => p(PFH:"Histone H2B Family",pmod(A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.051+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ATF2) => p(PFH:"Histone H2B Family",pmod(A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: 7. ATF2 H4/H2B Yeast to human Sequence-specific DNA-binding activator
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAG HO39-JQewciArwaTJtqcVGzWCtZITlHbya-KfOU1g
has assertion: a(CHEBI:gefitinib) =| kin(p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.054+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) =| kin(p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: A multitude of synthetic tyrosine kinase inhibitors have been developed and screened for potential preclinical activity, most of which reversibly compete with ATP for binding to the enzyme's intracellular catalytic domain. The quinazoline derivatives ZD1839 (gefitinib, Iressa) and OSI- 774 (erlotinib, Tarceva) appear to be the most promising to date. ZD1839 is a synthetic anilinoquinazoline [4-(3-chloro-4- fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy) quinazoline] that inhibits the EGFR tyrosine kinase, resulting in G1 cell cycle arrest and upregulation of the p27KIP1 cyclin dependent kinase inhibitor [88-91]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RANhuPKVDDOpV8E31pGlKWjKsDNMSYGuSdPro6I6T8WrA
has assertion: p(HGNC:AES) =| tscript(p(HGNC:AR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.055+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:AES) =| tscript(p(HGNC:AR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

5
value: AES amino-terminal enhancer of split Groucho/TLE family, represses AR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAH5OcXL-Z3W2gadw-fxAwHXj34oGKdpv-S6cx8KZN5a8
has assertion: complex(p(HGNC:EGF),p(HGNC:EGFR)) => kin(p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.066+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:EGF),p(HGNC:EGFR)) => kin(p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

7
value: Depsipeptide Depsipeptide was originally isolated from a strain of Chromobacterium violaceum. Initial studies with this bicyclic peptide demonstrated a selective decrease in c-myc expression. However, growth inhibition of the Ha-rastransformed NIH-3T3 clonal cell line Ras-1 was also observed in the absence of altered Ha-ras mRNA expression [67]. Depsipeptide appears to regulate the cell cycle at several points, including cell cycle arrest at G0/G1 and inhibition of signal transduction through mitogen-activated protein kinase (MAPK) with resultant p53-independent G1 arrest. EPIDERMAL GROWTH FACTOR RECEPTOR TYROSINE KINASE INHIBITORS Epidermal Growth Factor Receptor Binding by any member of the EGF family of ligands results in receptor dimerization and activation of the intracytoplasmic tyrosine kinase domain. In addition to homodimers, members of this receptor family can also form heterodimers through a series of complex interactions that result in transphosphorylation and the concerted regulation of the involved receptors. Six EGF-like ligands are known to bind and activate EGFR: EGF, TGF?, amphiregulin (cripto-1; CR-1), heparin-binding EGF (HB-EGF), betacellulin (BTC), and epiregulin (EPR) [78, 79]. Ligand binding to EGFR at the cell membrane triggers a signal transduction cascade that leads to the activation of nuclear transcription factors that promote cell division.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAP2pR2f17-ipTgkTgjM09vtATHTLYmdSuVYhakR5E050
has assertion: complex(p(HGNC:HBEGF),p(HGNC:EGFR)) => kin(p(HGNC:EGFR))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.069+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:HBEGF),p(HGNC:EGFR)) => kin(p(HGNC:EGFR))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

7
value: Depsipeptide Depsipeptide was originally isolated from a strain of Chromobacterium violaceum. Initial studies with this bicyclic peptide demonstrated a selective decrease in c-myc expression. However, growth inhibition of the Ha-rastransformed NIH-3T3 clonal cell line Ras-1 was also observed in the absence of altered Ha-ras mRNA expression [67]. Depsipeptide appears to regulate the cell cycle at several points, including cell cycle arrest at G0/G1 and inhibition of signal transduction through mitogen-activated protein kinase (MAPK) with resultant p53-independent G1 arrest. EPIDERMAL GROWTH FACTOR RECEPTOR TYROSINE KINASE INHIBITORS Epidermal Growth Factor Receptor Binding by any member of the EGF family of ligands results in receptor dimerization and activation of the intracytoplasmic tyrosine kinase domain. In addition to homodimers, members of this receptor family can also form heterodimers through a series of complex interactions that result in transphosphorylation and the concerted regulation of the involved receptors. Six EGF-like ligands are known to bind and activate EGFR: EGF, TGF?, amphiregulin (cripto-1; CR-1), heparin-binding EGF (HB-EGF), betacellulin (BTC), and epiregulin (EPR) [78, 79]. Ligand binding to EGFR at the cell membrane triggers a signal transduction cascade that leads to the activation of nuclear transcription factors that promote cell division.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAEJ CT6mmodP kvtikdInAXTDieHe7eo0RA6jU1AHAs
has assertion: a(SCHEM:Flavopiridol) =| kin(p(HGNC:CDK2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.077+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Flavopiridol) =| kin(p(HGNC:CDK2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: Flavopiridol (L-868275) is one of only two CDKIs to reach human clinical trials. It is a synthetic flavone, derived from the flavonoid rohitukine. It achieves antitumor activity through a variety of mechanisms, including inhibition of cell growth and proliferation, induction of apoptosis, and inhibition of angiogenesis. This agent is a broad spectrum phosphokinase inhibitor with the strongest activity against CDKs (specifically CDK1, CDK2, CDK4, CDK6, and CDK7), although interactions with the EGFR family of receptors, receptor associated protein kinases, and protein kinase C have also been reported
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAFuA D9Do0FnYmFte3X1Qf3QEQhzVls7Mi-CZp4QvI3s
has assertion: a(SCHEM:Flavopiridol) =| kin(p(HGNC:CDK6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.080+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Flavopiridol) =| kin(p(HGNC:CDK6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: Flavopiridol (L-868275) is one of only two CDKIs to reach human clinical trials. It is a synthetic flavone, derived from the flavonoid rohitukine. It achieves antitumor activity through a variety of mechanisms, including inhibition of cell growth and proliferation, induction of apoptosis, and inhibition of angiogenesis. This agent is a broad spectrum phosphokinase inhibitor with the strongest activity against CDKs (specifically CDK1, CDK2, CDK4, CDK6, and CDK7), although interactions with the EGFR family of receptors, receptor associated protein kinases, and protein kinase C have also been reported
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAFl fUsMFm5ar69pcDNUBjq Xpn133gxPr4TIQEPnwNk
has assertion: p(HGNC:NCOR2) =| tscript(p(EGID:6277))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.100+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NCOR2) =| tscript(p(EGID:6277))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

5
value: SMRT TRAC2 Represses unliganded TR, RAR, ER and PR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAIekGHLbhMNg7PufHxHz5TnV3ytPtISh50T3BUZvdnGg
has assertion: p(HGNC:NCOR2) =| tscript(p(HGNC:THRA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.102+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NCOR2) =| tscript(p(HGNC:THRA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

5
value: SMRT TRAC2 Represses unliganded TR, RAR, ER and PR
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAPRUrSXZJZYbg92nZEbIkakfMGfasVbAwLjn6jSbpJhE
has assertion: p(HGNC:NCOA3) => p(PFH:"Histone H3 Family",pmod(A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.104+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NCOA3) => p(PFH:"Histone H3 Family",pmod(A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

4
value: SRC-2/TIF-2/Grip1 ND SRC3 3/ACTR/AIB1/PCIP H3/H4
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAGKxuiOZz-m6ItUvtnIQ0lo6EliqwgKRvIhlu3mOnsvw
has assertion: a(SCHEM:Flavopiridol) -| cat(complex(NCH:"RNApo II Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.120+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Flavopiridol) -| cat(complex(NCH:"RNApo II Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

3
value: The inhibition of RNAP II by flavopiridol may contribute to apoptosis in a variety of cell lines and tumors.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAEzfCMyhUGMDrv1K37PryJwUAKD3ST5vw70t5JeH7EkA
has assertion: p(HGNC:SAP30) =| tscript(p(HGNC:THRA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.121+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SAP30) =| tscript(p(HGNC:THRA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320717

5
value: mSin3A Represses TR, RAR and others
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320717

RAFUNx3DsG3pBc5Mg3-rSrhhl1xCSChvQHQk8gDTlZXgo
has assertion: a(SCHEM:Pravastatin) -| p(HGNC:F3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.126+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Pravastatin) -| p(HGNC:F3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320841

3
value: However, until now, decreased TF expression, induced by statins, has been demonstrated solely on cultured human macrophages or monocytes [105].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320841

RAIs2eyaXO6NqJ0yHmS4YdZhX5p7s 7hJ61NssQLhy7so
has assertion: a(CHEBI:simvastatin) -| p(HGNC:F3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.128+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:simvastatin) -| p(HGNC:F3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15320841

3
value: However, until now, decreased TF expression, induced by statins, has been demonstrated solely on cultured human macrophages or monocytes [105].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15320841

RANMoxy8O1wnsJmaS- MiHiUqX0E2riLn8kNxK8FKQlF4
has assertion: a(SCHEM:Calcium) -| tscript(p(HGNC:HIF1A))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.132+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Calcium) -| tscript(p(HGNC:HIF1A))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15322093

4
value: Decreasing the intracellular calcium level by BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) induced HIF-1alpha nuclear accumulation and enhanced HIF-1 DNA binding within 1 h of incubation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15322093

RAEjyrbFOypTRHXVVvjiTLxZzAcRBK-nb0r0wwz0k2 KA
has assertion: cat(p(HGNC:AIFM1)) -> cat(p(HGNC:PARP1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.145+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AIFM1)) -> cat(p(HGNC:PARP1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15322527

6
value: Figure 2 | Extrinsic and intrinsic apoptotic signalling pathways in neurons. Black lines represent apoptotic pathways, blue lines represent survival pathways. The extrinsic death pathway is initiated by binding of the extracellular ligands, TNFa (tumour necrosis factor-a) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. TNFR1 activation leads to the formation of a TRADD RIP TRAF2 (TNF receptor death domain receptor interacting protein TNF associated factor 2) complex, which signals through the NFkB (nuclear factorkB) survival pathway (blue lines) or the JNK (cJun N teminal kinase)death pathway (black lines). RIP activates procaspase 2 and cleaves BID (BH3 (BCL2 (B-cell leukaemia/lymphoma-2) homology domain 3) interacting agonist). The TRADD FADD FLICE (TNF receptor death domain FAS associated death domain FADD like interleukin 1b) complex activates procaspase 8, triggering apoptosis through caspase 3 or cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8 or DAXX (death-associated protein )-mediated activation of JNK. JNK modifies BID to jBID, allowing its translocation to the mitochondrion and release of SMAC/DIABLO (second-mitochondrialderived activator of caspases). The intrinsic apoptotic pathway is initiated at the mitochondrion by diverse stimuli. Membrane permeabilization is mediated by BH3-only proteins, which sequester and inhibit the supression of BAX (B-cell lymphoma 2-associated protein X) by BCL2, allowing mitochondrial BAX translocation and the release of cytochrome c (Cyto c), SMAC/DIABLO, AIF (apoptosis-inducing factor) and HTRA2/OMI (high temperature requirement serine protease 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15322527

RALlg43cK3fteG WCXwbB1ETEb7Q7iQkB6bCtCynH319g
has assertion: tloc(p(HGNC:AIFM1),GOCCACC:"GO:0005739",GOCCACC:"GO:0005737") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.148+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(HGNC:AIFM1),GOCCACC:"GO:0005739",GOCCACC:"GO:0005737") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15322527

4
value: Figure 2 | Extrinsic and intrinsic apoptotic signalling pathways in neurons. Black lines represent apoptotic pathways, blue lines represent survival pathways. The extrinsic death pathway is initiated by binding of the extracellular ligands, TNFa (tumour necrosis factor-a) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. TNFR1 activation leads to the formation of a TRADD RIP TRAF2 (TNF receptor death domain receptor interacting protein TNF associated factor 2) complex, which signals through the NFkB (nuclear factorkB) survival pathway (blue lines) or the JNK (cJun N teminal kinase)death pathway (black lines). RIP activates procaspase 2 and cleaves BID (BH3 (BCL2 (B-cell leukaemia/lymphoma-2) homology domain 3) interacting agonist). The TRADD FADD FLICE (TNF receptor death domain FAS associated death domain FADD like interleukin 1b) complex activates procaspase 8, triggering apoptosis through caspase 3 or cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8 or DAXX (death-associated protein )-mediated activation of JNK. JNK modifies BID to jBID, allowing its translocation to the mitochondrion and release of SMAC/DIABLO (second-mitochondrialderived activator of caspases). The intrinsic apoptotic pathway is initiated at the mitochondrion by diverse stimuli. Membrane permeabilization is mediated by BH3-only proteins, which sequester and inhibit the supression of BAX (B-cell lymphoma 2-associated protein X) by BCL2, allowing mitochondrial BAX translocation and the release of cytochrome c (Cyto c), SMAC/DIABLO, AIF (apoptosis-inducing factor) and HTRA2/OMI (high temperature requirement serine protease 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15322527

RAMslM247BmAHTTJJapOyBoHM1LWjTYZzRcVelYhmkEM4
has assertion: tloc(p(HGNC:HTRA2),MESHCL:Mitochondria,MESHCL:Cytoplasm) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.150+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(HGNC:HTRA2),MESHCL:Mitochondria,MESHCL:Cytoplasm) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15322527

4
value: Figure 2 | Extrinsic and intrinsic apoptotic signalling pathways in neurons. Black lines represent apoptotic pathways, blue lines represent survival pathways. The extrinsic death pathway is initiated by binding of the extracellular ligands, TNFa (tumour necrosis factor-a) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. TNFR1 activation leads to the formation of a TRADD RIP TRAF2 (TNF receptor death domain receptor interacting protein TNF associated factor 2) complex, which signals through the NFkB (nuclear factorkB) survival pathway (blue lines) or the JNK (cJun N teminal kinase)death pathway (black lines). RIP activates procaspase 2 and cleaves BID (BH3 (BCL2 (B-cell leukaemia/lymphoma-2) homology domain 3) interacting agonist). The TRADD FADD FLICE (TNF receptor death domain FAS associated death domain FADD like interleukin 1b) complex activates procaspase 8, triggering apoptosis through caspase 3 or cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8 or DAXX (death-associated protein )-mediated activation of JNK. JNK modifies BID to jBID, allowing its translocation to the mitochondrion and release of SMAC/DIABLO (second-mitochondrialderived activator of caspases). The intrinsic apoptotic pathway is initiated at the mitochondrion by diverse stimuli. Membrane permeabilization is mediated by BH3-only proteins, which sequester and inhibit the supression of BAX (B-cell lymphoma 2-associated protein X) by BCL2, allowing mitochondrial BAX translocation and the release of cytochrome c (Cyto c), SMAC/DIABLO, AIF (apoptosis-inducing factor) and HTRA2/OMI (high temperature requirement serine protease 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15322527

RAH52g0s4ygXxx2k1hgGl4FkPQagZSCFodF8AZfHv3LMk
has assertion: kin(p(HGNC:MAP3K5)) -> kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.157+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP3K5)) -> kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15322527

6
value: Figure 4 Anti-apoptotic brakes at the mitochondrion. Black lines represent apoptotic pathways, red lines indicate inhibition. BCL2 (B-cell leukaemia lymphoma-2) and ?B-crystallin prevent mitochondrial release of the apoptogenic factors AIF (apoptosisinducing factor), cytochrome c (cyto c), HTRA2/OMI (high temperature requirement serine protease 2) and SMAC/DIABLO (second-mitochondrial-derived activator of caspases) into the cytosol by the binding and sequestration of BAX (B-cell lymphoma 2-associated protein X) and pro-apoptic BCL2 BAX-like molecules, BAK (BCL2 agonist killer 1) and BOK (BCL2-related ovarian killer protein) in the cytosol. APC (activated protein C) might prevent AIF release by increasing BCL2 expression. BAX translocation to the outer mitochondrial membrane is prevented by HSP70 (heat shock protein 70) and its co-chaperone HSP40(DNAJL1/DNAJL2). Meanwhile, membrane depolarization is prevented by the uncoupling properties of UCP2 (uncoupling protein 2) and the free radical scavenging properties of GIF (growth inhibitory factor). BH3, BCL2 homology domain 3; cIAP1, cellular apoptosis inhibitor 1; ENDOG, endonuclease G; HSP27, heat shock protein 27; IAP, inhibitor of apoptosis protein; XIAP, X-chromosome linked inhibitor of apoptosis protein.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15322527

RAPrRVB1M9TFDmeEXo98a7InoLKwADmd5iSnUYfHRCHas
has assertion: kin(p(HGNC:SRC)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.162+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:SRC)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15326164

4
value: Oxaliplatin-induced apoptosis, potentiated by kinase-defective c-Src mutants, was dependent on activation of caspase 8 and associated with Bid cleavage.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15326164

RAJjytctXyrwT4A6ZWaYaTViunRiPP8KtqAx7QWPmRtP4
has assertion: a(SCHEM:Calcium) -> tscript(p(HGNC:CREB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.164+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Calcium) -> tscript(p(HGNC:CREB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15326191

4
value: CREB and NFkappaB were activated most likely in response to an observed elevation in cytosolic calcium
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15326191

RAJ0qiFIH2aQ70poDBjOJ33afHZZ26j4uTc1EVU11MvwQ
has assertion: p(MGI:Nfatc2ip) -> tscript(p(MGI:Nfatc2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.169+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Nfatc2ip) -> tscript(p(MGI:Nfatc2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15327772

5
value: Arginine methylation of the amino terminus of NIP45 modulated its interaction with NFAT and resulted in augmented cytokine production, while T cells from mice lacking NIP45 had impaired expression of IFNgamma and IL-4.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15327772

RAPSohZ98XsY0XSq7FdYRMmZivNX-ru0hXYK2rdVMI4zc
has assertion: p(HGNC:PEBP1) -| (tscript(complex(NCH:"Nfkb Complex")) -| bp(MESHPP:Apoptosis))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.176+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PEBP1) -| (tscript(complex(NCH:"Nfkb Complex")) -| bp(MESHPP:Apoptosis))
label: tscript(complex(NCH:"Nfkb Complex")) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15327891

5
value: RKIP has been shown to disrupt the Raf-1-MEK1/2 [mitogen-activated protein kinase-ERK (extracellular signal-regulated kinase) kinase-1/2]-ERK1/2 and NF-kappaB signaling pathways, via physical interaction with Raf-1-MEK1/2 and NF-kappaB-inducing kinase or transforming growth factor beta-activated kinase-1, respectively, thereby abrogating the survival and antiapoptotic properties of these signaling pathways.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15327891

RAKfl88VSw8eTbX9a37Ho0fJDhSJqYHaiFhqJ4UzxOAhY
has assertion: kin(p(HGNC:MAPK1)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.179+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK1)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15327891

4
value: RKIP has been shown to disrupt the Raf-1-MEK1/2 [mitogen-activated protein kinase-ERK (extracellular signal-regulated kinase) kinase-1/2]-ERK1/2 and NF-kappaB signaling pathways, via physical interaction with Raf-1-MEK1/2 and NF-kappaB-inducing kinase or transforming growth factor beta-activated kinase-1, respectively, thereby abrogating the survival and antiapoptotic properties of these signaling pathways.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15327891

RAN lC3E Z0fjO8PsH1uVXTQvkIu02n OwBW-YiEcOyyY
has assertion: a(SCHEM:Phenyldichloroarsine) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Phenyldichloroarsine) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15328416

2
value: The recently discovered mitochondrial and nuclear Grx (Grx2) differs from the more abundant cytosolic Grx (Grx1) by its higher affinity toward S-glutathionylated proteins and by being a substrate for thioredoxin reductase. Here, we have successfully established a method to silence the expression of Grx2 in HeLa cells by using short interfering RNA to study its role in the cell. Cells with levels of Grx2 of the control were dramatically sensitized to cell death induced by doxorubicin/adriamycin and phenylarsine oxide but did not show signs of a general increase in oxidative damage with respect to carbonylation and glutathionylation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15328416

RAORCje4Qr0y2uUKdePHDlQg2oIgkHWUMc0YrdDzMuwo8
has assertion: tscript(p(MGI:Mkl1)) -> p(MGI:Ereg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.197+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Mkl1)) -> p(MGI:Ereg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15329155

5
value: wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15329155

RAJkYWI7s7sgtlMOcUzUjeGEk3 We3vAIKqUs-7ss6h-c
has assertion: tscript(p(MGI:Mkl1)) -> p(MGI:Mat2a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.205+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Mkl1)) -> p(MGI:Mat2a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15329155

5
value: wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15329155

RAK-U8kLEipO1sgNTxSQCLYAIEmTVq2 XeOHmmmVRR-A4
has assertion: tscript(p(MGI:Mkl1)) -> p(MGI:Trib1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.210+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Mkl1)) -> p(MGI:Trib1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15329155

5
value: wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15329155

RAHQm3NymBV15T8Uvcy6Wuy1ObJdnQK1YcooIotV4wpDQ
has assertion: a(CHEBI:progesterone) -> r(MGI:Esr1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -> r(MGI:Esr1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15329476

3
value: Treatment with progesterone (P4) resulted in the induction of CaBP-9k mRNA, and a co-treatment with estrogen (E2) plus P4 evoked a synergic effect on its mRNA level in this tissue. translation of CaBP-9k protein was enhanced by E2, while no difference was observed at the transcriptional level. E2 stimulated the expression levels of ERalpha and PR mRNAs and P4 inhibited the expression of these transcripts at an early time point (12 h) and increased them at 24 and 48 h
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15329476

RAMirmcSo9CbhzHnD9GCP89dBq-vkZLuIMRCOCZhjpB8Y
has assertion: p(MGI:Pik3r1) -| p(MGI:Lep)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.217+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Pik3r1) -| p(MGI:Lep)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15331535

4
value: On the normal diet, serum leptin levels of Pik3r1(-/-) mice were significantly higher than in wild-type mice as a result of increased leptin secretion from adipocytes, presumably due to the increased PtdIns(3,4,5)P3 production in adipocytes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15331535

RAMwll 5tm2p7ESQHPyQ0NEBdtf6PCIhdeS8zUuC4m1Y4
has assertion: p(RGD:Fgf7) -> p(RGD:Cdc25a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.227+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Fgf7) -> p(RGD:Cdc25a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15333329

4
value: KGF alone greatly stimulated proliferation and increased cyclin-dependent kinase (cdk) 2 kinase activity and Retinoblastoma susceptibility gene product (Rb) phosphorylation. Cyclin D1, cdk2, and cdc25A protein levels were increased, and p15(Ink4b) and p27(Kip1) protein levels were decreased. (KGF = FGF7)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15333329

RAG7UyBgBVC3OKsyNHfPoZUeSxetAUjgXuRAnNQu8GlEA
has assertion: p(RGD:Fgf7) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.234+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Fgf7) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15333329

3
value: TGF-beta inhibits the proliferative effect of KGF in vitro and may be a biologic antagonist of KGF.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15333329

RAKZNkK0h8xn QPMpbaeG6lQVARN8AA4 iy4LRvCzTS-s
has assertion: bp(GO:"response to hypoxia") -| r(RGD:Cdc25a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.237+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| r(RGD:Cdc25a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15333578

3
value: In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15333578

RAOQVzcKLk3OY5KsH6ByBWtVDEG y--C1YLJClygSQu3A
has assertion: cat(p(RGD:Tlr4)) -> path(MESHD:Ischemia)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.244+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Tlr4)) -> path(MESHD:Ischemia)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15334694

4
value: TLR4 and its partner molecule MD-2 may play an important role in Kupffer cell activation and IR injury.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15334694

RAHNoWjeWpWkdTbjV67r5rP5Hk7iIvJ4PwCGoB2uM4IK4
has assertion: gtp(p(HGNC:RHEB)) -> kin(p(HGNC:RPS6KB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.262+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:RHEB)) -> kin(p(HGNC:RPS6KB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15340059

6
value: Rheb to stimulate S6 kinase (S6K) phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15340059

RAGrZWE4k1XDW 34xEjddeqGQfHg4GdZ4MnuW46X2gFQU
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Meis1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.265+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Meis1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15340120

3
value: Fig. 3A. Genes identified in differentiation pattern 2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15340120

RAKKxAs86ziHpONsHMsSyUQm48ylVwt-SkJ1pGkCPCpPs
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Nr2f1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.266+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Nr2f1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15340120

3
value: Fig. 3A. Genes identified in differentiation pattern 2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15340120

RANshUnUB0vZven0O8Ux3c4UdHFvITFV2cQW-83wajo4Y
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Acta2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.272+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Acta2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15340120

3
value: Fig. 5. Genes identified in differentiation pattern 4
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15340120

RAPlPQiuxMMZdiJKPiWrX1xIT78t8cMuhKmj3RtAqz2Jo
has assertion: p(HGNC:SPRY1) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.295+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SPRY1) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15342396

3
value: We investigated Spry expression levels in various cancers and found that Spry1 and Spry2 were down-regulated consistently in breast cancers.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15342396

RAKlC1 blpV16zlQotkd0lSOAzyFp201OYrkgfgkH1Z0I
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -> tport(p(HGNC:KPNA2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.300+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")) -> tport(p(HGNC:KPNA2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15342649

5
value: First, AMPK triggered the acetylation of importin alpha1 on Lys(22), a process dependent on the acetylase activity of p300. Second, AMPK phosphorylated importin alpha1 on Ser(105)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15342649

RAFe5qtzEdTckbl5FRT0hvApSVlHwBlkYW8gdToZ S6gk
has assertion: tloc(p(HGNC:ELAVL1),GOCCACC:"GO:0005737",GOCCACC:"GO:0005634") -> cat(p(HGNC:ELAVL1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.302+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(HGNC:ELAVL1),GOCCACC:"GO:0005737",GOCCACC:"GO:0005634") -> cat(p(HGNC:ELAVL1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15342649

6
value: Here, we provide evidence that importin alpha1, an adaptor protein involved in nuclear import, contributes to the nuclear import of HuR through two AMPK-modulated mechanisms
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15342649

RANkj8VDW1cHyTAdZctCZhsSA0707ox7UpBa3nUgoJBMc
has assertion: a(CHEBI:troglitazone) -> r(RGD:Slc2a4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.308+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:troglitazone) -> r(RGD:Slc2a4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15345487

3
value: TG (50 microM) induced GLUT4 and h-caldesmon expression in 24-h culture of explanted carotid arteries of DOCA salt-hypertensive rats,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15345487

RAMd5q6UVJHDITzIiJLpyuWB XhxapE O6V1JtO1707Mw
has assertion: p(MGI:Hey2) -> p(MGI:Arhgef2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.311+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Hey2) -> p(MGI:Arhgef2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15345511

4
value: Although total Rac1 protein was not changed in KO VSMCs, the level of the Rac guanine exchange factor (GEF), Sos1, was decreased.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15345511

RAER9- aNZ-rxgKPkLmtnbcAWu7EHR4IPWNssVxjlYcVk
has assertion: a(CHEBI:estradiol) -> r(MGI:Txnrd3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.317+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(MGI:Txnrd3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15345672

3
value: we then determined the mRNA levels of Txn1 and the Txnrd3 genes and found that these levels also increased after E2 treatment, with approximately 4-fold induction at the 24-h point for Txn1 and 2.5-fold induction for Txnrd3
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15345672

RAOTbi1gFnyzAK8vh5vgRA04J3p0R77JIi2qCQuWCiQLw
has assertion: tscript(complex(NCH:"Nfkb Complex")) -> r(HGNC:NUAK2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.324+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCH:"Nfkb Complex")) -> r(HGNC:NUAK2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15345718

4
value: We demonstrate that up-regulation of SNARK in response to CD95 ligand and tumor necrosis factor alpha depends on activation of NF-kappaB.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15345718

RAMRNu70Qv1gsakkXhD3b6WwRcbQ1eR6Ak2bhkPq2p93w
has assertion: cat(p(HGNC:BAK1)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.350+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:BAK1)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15353788

4
value: BID induces oligomerization of proapoptotic members BAX and BAK, resulting in release of cytochrome c from mitochondria and subsequent induction of apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15353788

RAHBbIzIU83aORcHXdbOPI8yxqZ-FHmoYCEu0KpbjGDvk
has assertion: gtp(p(MGI:Kras)) -> cat(p(MGI:St6gal1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.356+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(MGI:Kras)) -> cat(p(MGI:St6gal1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15355339

6
value: The accumulation of the ST6Gal I transcript in response to activated Ras was accompanied by an increase of alpha2,6-sialyltransferase activity and of Neu5Acalpha2,6Gal at the cell surface.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15355339

RAFdtJDmDOcms8Y2rVznRXiKA84OHAqqWh3yZ0cnuW4 I
has assertion: p(HGNC:MAPK11,pmod(P)) -> tscript(p(HGNC:ATF2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.372+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MAPK11,pmod(P)) -> tscript(p(HGNC:ATF2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356147

5
value: HDAC3 decreases the MAPK11 phosphorylation state and inhibits the activity of the MAPK11-dependent transcription factor, activating transcription factor-2 (ATF-2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356147

RAOp-e2hH3-xUamVBqyTdtr5Jp9KbL8SfNb105v 1p3AQ
has assertion: a(CHEBI:lipopolysaccharide) -> r(HGNC:TNF)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.375+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(HGNC:TNF)
label: p(HGNC:HDAC3) -| (a(CHEBI:lipopolysaccharide) -> r(HGNC:TNF))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356147

5
value: HDAC3-repressed TNF gene expression, and TNF protein production observed in response to LPS stimulation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356147

RALX2B6mMhYIi-jlMkRJqbKmTwIie vUni0Pawl53FQGY
has assertion: a(CHEBI:lipopolysaccharide) -> tscript(p(HGNC:ATF2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.383+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> tscript(p(HGNC:ATF2))
label: p(HGNC:HDAC3) -| (a(CHEBI:lipopolysaccharide) -> tscript(p(HGNC:ATF2)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356147

6
value: LPS-mediated activation of ATF-2 was inhibited by HDAC3 in a time- and dose-dependent manner.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356147

RALv2Ma5MBDQn38j5TXExjsgKe2X16xfosO3N-90mHB5s
has assertion: p(HGNC:RGS19) -| cat(p(HGNC:DRD2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.391+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:RGS19) -| cat(p(HGNC:DRD2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356268

5
value: Pleiotropic G proteins are essential for the action of hormones and neurotransmitters and are activated by stimulation of G protein-coupled receptors (GPCR), which initiates heterotrimer dissociation of the G protein, exchange of GDP for GTP on its Galpha subunit and activation of effector proteins. Regulator of G protein signaling (RGS) proteins regulate this cascade and can be recruited to the membrane upon GPCR activation. Direct functional interaction between RGS and GPCR has been hypothesized. We show that recruitment of GAIP (RGS19) by the dopamine D2 receptor (D2R), a GPCR, required the scaffold protein GIPC (GAIP-interacting protein, C terminus) and that all three were coexpressed in neurons and neuroendocrine cells. Dynamic translocation of GAIP to the plasma membrane and coassembly in a protein complex in which GIPC was a required component was dictated by D2R activation and physical interactions. In addition, two different D2R-mediated responses were regulated by the GTPase activity of GAIP at the level of the G protein coupling in a GIPC-dependent manner. Since GIPC exclusively interacted with GAIP and selectively with subsets of GPCR, this mechanism may serve to sort GPCR signaling in cells that usually express a large repertoire of GPCRs, G proteins, and RGS.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356268

RAJhWvmJb7sGIF B-2uSkA9lLtYJlYeEL5r-oxC3z QgE
has assertion: cat(p(HGNC:TNFRSF10B)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.394+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:TNFRSF10B)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356269

4
value: TRAIL (TNF-related apoptosis-inducing ligand) death receptors DR4 and DR5 facilitate the selective elimination of malignant cells through the induction of apoptosis. From previous studies the regulation of the DR4 and DR5 cell-death pathways appeared similar; nevertheless in this study we screened a library of small interfering RNA (siRNA) for genes, which when silenced, differentially affect DR4- vs. DR5-mediated apoptosis. These experiments revealed that expression of the signal recognition particle (SRP) complex is essential for apoptosis mediated by DR4, but not DR5. Selective diminution of SRP subunits by RNA interference resulted in a dramatic decrease in cell surface DR4 receptors that correlated with inhibition of DR4-dependent cell death. Conversely, SRP silencing had little influence on cell surface DR5 levels or DR5-mediated apoptosis. Although loss of SRP function in bacteria, yeast and protozoan parasites causes lethality or severe growth defects, we observed no overt phenotypes in the human cancer cells studied--even in stable cell lines with diminished expression of SRP components. The lack of severe phenotype after SRP depletion allowed us to delineate, for the first time, a mechanism for the differential regulation of the TRAIL death receptors DR4 and DR5--implicating the SRP complex as an essential component of the DR4 cell-death pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356269

RAPFHPQkMCVMuEnww9IeHubGvL148GdD ddM9T1HGMi10
has assertion: p(HGNC:CLK1) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.396+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CLK1) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356269

3
value: siRNAs that inhibit or enhance DR4- or DR5-mediated cell death
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356269

RAKHl 7Ch7p8u f SrgI vEl5euCoimtNo5-WSdViH Oc
has assertion: p(HGNC:VPS39) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.406+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:VPS39) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356269

3
value: siRNAs that inhibit or enhance DR4- or DR5-mediated cell death
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356269

RAJ2mHzmaCpaRtrUv1 Xjr63Ku-NdpLQ3wrV3MYonBJOQ
has assertion: complex(p(HGNC:PPARA),p(HGNC:RXRA)) => (tscript(p(HGNC:MEF2C)) => r(HGNC:CPT1B))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.407+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:PPARA),p(HGNC:RXRA)) => (tscript(p(HGNC:MEF2C)) => r(HGNC:CPT1B))
label: tscript(p(HGNC:MEF2C)) => r(HGNC:CPT1B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15356291

9
value: synergistic activation of the CPT1beta gene promoter by MEF2C and PPARalpha-RXRalpha
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15356291

RAIn8gAB1SqiTfprnk408dYvwfYEN3zsLQ5Uk653jPXO8
has assertion: p(RGD:Ins1) -> kin(p(RGD:Mapk3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.456+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Ins1) -> kin(p(RGD:Mapk3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15358516

5
value: Inhibition of MEK1 significantly inhibited extracellularly regulated kinase (ERK)1/2 activation and insulin-regulated Gene33 transcription and protein
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15358516

RAIoZ1ntaP7eh8HOyGwJAgWVOSc9KM5vgY8amgEnugtIE
has assertion: p(RGD:Nr0b2) -| tscript(p(RGD:Foxa3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.468+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Nr0b2) -| tscript(p(RGD:Foxa3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15358835

5
value: Transient transfection assay demonstrated that SHP inhibited the transcriptional activity of all three isoforms of HNF3, HNF3alpha, beta, and gamma.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15358835

RALPrsh7AbSEU1CpkcoXaR7TOL7XqXJiZkJK7uULsHvXA
has assertion: a(SCHEM:"NS 398") -| cat(p(MGI:Ptgs2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.473+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"NS 398") -| cat(p(MGI:Ptgs2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15358864

4
value: Theseeffects were reversed by NS398, a COX-2-specific inhibitor, suggesting thatlipopolysaccharide-mediated inhibition of CUGBP2 is a PG-dependent mechanism.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15358864

RANXjk bGnquMnkHbpJ8rlq6gbiFswmTQtwP0DbduQft4
has assertion: path(SDIS:"food intake") -| r(MGI:Caprin1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.475+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(MGI:Caprin1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15361355

3
value: To investigate the mechanisms underlying long-term resistance of the A/J mouse strain to diet-induced obesity, we studied, over a period of 4 wk, the expression of uncoupling proteins in brown adipose tissue and the expression of hypothalamic neuropeptides known to regulate energy homeostasis and then used microarray analysis to identify other potentially important hypothalamic peptides. (Table 2- 1 week)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15361355

RAPfJpzqcsGonAa8cw5sE1JfeS4ougbfoWKVRzuDs KGs
has assertion: path(SDIS:"food intake") -| r(MGI:Tiam1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.495+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(MGI:Tiam1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15361355

3
value: To investigate the mechanisms underlying long-term resistance of the A/J mouse strain to diet-induced obesity, we studied, over a period of 4 wk, the expression of uncoupling proteins in brown adipose tissue and the expression of hypothalamic neuropeptides known to regulate energy homeostasis and then used microarray analysis to identify other potentially important hypothalamic peptides. (Table 2- 1 week)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15361355

RAMonZgxJYVGXhJfkui2ADAYNl7st5flP8S7w3DWh-LPo
has assertion: tscript(p(HGNC:TP63)) -> r(HGNC:ITGA3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.501+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP63)) -> r(HGNC:ITGA3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15361520

5
value: We describe here identification of ITGA3 encoding integrin alpha(3) as a target of its trans-activating function, proposing that p51/p63 allows epidermal stem cells to express laminin receptor alpha(3)beta(1) for anchorage to the basement membrane.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15361520

RAPAhBjJh8WWEphpvO8WvNDveWHCLm76R44DyK4r0-GHw
has assertion: bp(GO:"response to heat") -> tloc(p(HGNC:HSF1),GOCCACC:"GO:0005737",GOCCACC:"GO:0005634")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.529+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to heat") -> tloc(p(HGNC:HSF1),GOCCACC:"GO:0005737",GOCCACC:"GO:0005634")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15364926

4
value: The effects of 14-3-3epsilon binding on HSF1 were complex, however, depending on extracellular conditions, in that HSF1-14-3-3 binding at 37 degrees C led to the cytoplasmic sequestration and repression of HSF1, whereas heat shock overrode these effects and caused quantitative nuclear localization of HSF1. Although the effects of 14-3-3epsilon binding to HSF1 were overridden acutely by stress
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15364926

RAErn48VlgBobaIogHrdp7C9fFH9QoLSLNdKkVnl4gFMw
has assertion: complex(p(HGNC:HSF1),p(HGNC:MAPK3)) -> kin(p(HGNC:MAPK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.530+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:HSF1),p(HGNC:MAPK3)) -> kin(p(HGNC:MAPK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15364926

7
value: We have found that the two pathways interact directly and that heat shock causes the physical association of ERK1 with HSF1, an interaction that promotes the kinase activity of ERK in heat-shocked cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15364926

RAMHNpsfZUfqio1qO2EmoVzV09tegvglL-cJs5Asv6SEA
has assertion: cat(p(MGI:Chd8)) =| tscript(p(MGI:Ctnnb1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.550+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Chd8)) =| tscript(p(MGI:Ctnnb1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15367660

6
value: Duplin (axis duplication inhibitor) interacts with beta-catenin and prevents its binding to Tcf, thereby inhibiting downstream Wnt signaling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15367660

RAH68yGkT3nuhYBtNsyuDq7ygvpfVZPKWMRdRrh1HVgTs
has assertion: kin(p(HGNC:ERBB2)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.561+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ERBB2)) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15367686

5
value: In this report we have explored the mechanism linking the loss of expression of ERalpha in breast cancer cells with overexpression of Her-2/neu, which signals constitutively via a phosphatidylinositol 3-kinase (PI3K)/Akt kinase pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15367686

RAJ0bnNaKLDgvgSB0sDMCUnCE1PuS GctdbJK2VUYodMY
has assertion: p(HGNC:ATF2,pmod(P)) => tscript(p(HGNC:ATF2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.591+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ATF2,pmod(P)) => tscript(p(HGNC:ATF2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15371457

5
value: the transcriptional activity of the ATF-2 transcription factor, as a direct p38 and JNK target in syndecan-4-null and wild type cells. In the absence of syndecan-4, both ATF-2 phosphorylation and transcriptional activity were significantly more elevated compared with wild type cells, and both activities were decreased either by the re-expression of syndecan-4 or by the expression of RacN17.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15371457

RAEMrlkUEPO9vh5Jdv6Rmua6MhJ2IUqnS3wmfBqcUJuSM
has assertion: a(CHEBI:estradiol) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.605+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/1537279

2
value: In these cells, exposure to the synthetic glucocorticoid dexamethasone (DEX) markedly decreases basal as well as 17 beta-estradiol (E2)-induced cellproliferation while causing a maximal 10-fold stimulation of apo-D secretion inthe presence or absence of E2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/1537279

RAIwVdnMmY3xBIxZKWp-AZvs2uPbYC1mV-PRDelepz iw
has assertion: bp(GO:"response to hypoxia") -| r(HGNC:BRCA1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.607+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| r(HGNC:BRCA1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAIuNpx85bKVeWoFX2fXaeWOcxnBDudqf0EoB2fD 9l0w
has assertion: bp(GO:"response to hypoxia") -| r(HGNC:CDC6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.608+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| r(HGNC:CDC6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAG1udIAUiVpK5hYUgGNTLXiw25BRhY9uSwKMNhUSalcg
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:BHLHE40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.624+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:BHLHE40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAP-WKvSoQEA9yw9LWQngYLf0OdyxjNnFzm2iUc0Vi1G4
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:CDKN1C)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.626+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:CDKN1C)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAL MSuG0g-K- jIOEgkrAnyLMzKUR kfS4l2nmrU4kDA
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:COL9A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.629+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:COL9A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAMK2FNAycbrMQRQ2r57n5mpxIfzb-pU5FaZM0cpr5-Vo
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:CXCR4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.631+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:CXCR4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAFyqtWh5xmQ-NdhU2GDqiGZeKcg8ry1IY9bozbkD dkw
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:ERO1L)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.637+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:ERO1L)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAEOyxdrkr-SenplwZI D5UWl- XYpNGYO1LWhpi1re6o
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:INHBA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.644+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:INHBA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAMRPK-qAE1D5cdPEKl60lzSDDjaTc7j5HrRPJfI1DLWY
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:MEF2A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.652+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:MEF2A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RALV2eOm94KXW7RaBYv2nLRt8tv0m PxKBcJeX74YzUhM
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:P4HA2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.658+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:P4HA2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RALZe8qhrMEqQLLZQIcLk0-YEFunl 1g8F-emcpuQRrTI
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:PGF)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.664+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:PGF)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAGQ0BaTjduJbMlX1KJZeGk6h0TXuUSFbNeUJd3YaW3q4
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:STC2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.667+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:STC2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAOPbWZrlGSJo4QfVxOE9gykP1JQtg7jykHmA0CbFGRMU
has assertion: bp(GO:"response to hypoxia") -> r(HGNC:TXNIP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.672+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> r(HGNC:TXNIP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374877

3
value: Hypoxia-inducible factor 1 (HIF-1) activates transcription of genes encoding angiogenic growth factors, which are secreted by hypoxic cells and stimulate endothelial cells, leading to angiogenesis. To determine whether HIF-1 also mediates cell-autonomous responses to hypoxia, we have compared gene expression profiles in arterial endothelial cells cultured under nonhypoxic versus hypoxic conditions and in nonhypoxic cells infected with adenovirus encoding beta-galactosidase versus a constitutively active form of HIF-1alpha (AdCA5). There were 245 gene probes that showed at least 1.5-fold increase in expression in response to hypoxia and in response to AdCA5; 325 gene probes showed at least 1.5-fold decrease in expression in response to hypoxia and in response to AdCA5. The largest category of genes down-regulated by both hypoxia and AdCA5 encoded proteins involved in cell growth/proliferation. Many genes up-regulated by both hypoxia and AdCA5 encoded cytokines/growth factors, receptors, and other signaling proteins. Transcription factors accounted for the largest group of HIF-1-regulated genes, indicating that HIF-1 controls a network of transcriptional responses to hypoxia in endothelial cells. Infection of endothelial cells with AdCA5 under nonhypoxic conditions was sufficient to induce increased basement membrane invasion and tube formation similar to the responses induced by hypoxia, indicating that HIF-1 mediates cell-autonomous activation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374877

RAHNHnxAIYBw9 14efcWHZVFD4s7QYHpzer S0mRfz3Xk
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Ccne2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.691+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Ccne2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RANSZXiI9Y mW82NdsAQeY2kNHnWfG MQuTPxRcnWBacw
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Eif4g2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.711+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Eif4g2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAJY59pj2-D3fQI8FZpmgnQ5GnvpcGKr8-YgzTh7CXpiI
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Hmgb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.718+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Hmgb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RANZp62PQkIbnsUGnnw1Jn yrS2NYkcVogNuYCDg1QoOg
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Lcn2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Lcn2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAJnsSWCEQJTMiASm2kIwE2dqzwrEEuCnNQFDn1XokP5w
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Nrk)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.730+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Nrk)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RALjWoCgWEFPu8MRCfen4YXz8Rs9b9ROLforaWIWYeOmI
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Rock1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.739+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Rock1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAGkOlprv4CLnyeNktiZN4KJrizINpibSqtf32Ccwh2p8
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Rabep1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.741+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Rabep1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAHBzT0nthYPWztqurAJXk0Bgz-g JQHtZJL5-IX70hvY
has assertion: tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Serinc1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.746+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -| r(MGI:Serinc1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAI5L-B9cPm44boNvzmS54W2zvkdXvqgVKSwlixfchIrM
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Bok)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.767+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Bok)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAFPAeOhFJ2ELowjMSxwX6T45ZmBlwis2MJ5Jjx9 yb4o
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Capza2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.771+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Capza2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAIzF1DUUN4niQSz2BJrc92xKG1ESAzJFvnZBoB1CSavQ
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Cd97)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.773+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Cd97)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RALy vvtQ3RLxOSmpRKAk6dBxpo p4aMAxZ3yYxvfOPq0
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Cdh3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.775+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Cdh3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAFxg9CoL03amOaHDaI2LIf5Rgbxt7d6H2pBbG7wyVurs
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Ly6e)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.815+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Ly6e)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAMBGEfxzhlEbAX9VCO8wqt9Zuke9byiW0M0EtVEAAhQI
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Myc)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.825+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Myc)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAJzkRtdHXRz3WEARy8OGqeMxY2tfSqd4CbJehMzCYIJ8
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Nfkb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.826+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Nfkb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAKhZdaTwsCR2C9k80X4a7snwSFe8e1USKmoW9LOU-zG4
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Pdlim1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.830+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Pdlim1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAKVLTzI5nQfPwwbXrff4wVfAdRmuHMjfQgBKkyNATvEs
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Ppp3cb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.834+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Ppp3cb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RANhEfob3v2uLwRrSTmFPqdhlAHNwY-c7kAeWd4aK5GLg
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Pik3r1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.840+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Pik3r1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAKPveL-0NqibX66JG8BcOcY7d3M4dbic3Bz53qhg0dI8
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rpsa)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.844+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rpsa)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAEEXTyb5KiWLIN-fhqDJFSaFD9DONvzkeceIEHtVxp7c
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rps2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.850+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rps2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RALm1-30hB0GcJqmv7BZc2l62mfexTOMiIcLezq-HXo2A
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Sdc1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.892+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Sdc1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAPzdt4FRSqgNdPGKhs5Fdb3lgbO4E6Wc79Sjj-xVzk5Q
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Slc12a2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.895+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Slc12a2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAJoikC6ixUQ1 rdiJS6FfqzZiRbKAuSoQ3cUG-Ba8sxE
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Tgfb1i1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.901+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Tgfb1i1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15374962

4
value: We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15374962

RAMGGs3Xfk b0OsdqC5Tz9KGB1YWMV10uUVZXTHELsxns
has assertion: p(HGNC:DCTN1) -> (p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.917+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:DCTN1) -> (p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P)))
label: p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375157

6
value: Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375157

RAFqvUbjXQ-OHpHAdvwKlk1Zb2hgCiSI33VIFyVfCAy1U
has assertion: p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.925+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375157

4
value: Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375157

RAL-FNSLxvJnHEbhMo-scMseUUbj3QzYLcAHdrVKMJcMk
has assertion: p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.927+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375157

4
value: Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375157

RAGUpqHrad RjrUrFeKCjn5ys092OedgWuP45nFv5u4vs
has assertion: p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.933+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:MAP2K6,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375157

4
value: Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375157

RANtWEPx5-GnUcii3i8UCEcrOJHl7mK225aabh5myd3 g
has assertion: p(HGNC:TNF) -> p(HGNC:MAP2K3,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.940+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:MAP2K3,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375157

4
value: Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375157

RALp8TdrTatNwHQtaLw6KZmySiETc8UrjaHuzVdpNED1I
has assertion: p(EGID:183) -> r(HGNC:NR4A2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.954+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:183) -> r(HGNC:NR4A2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375197

4
value: #------------------------------------------------------------------------------- Eleven genes were found to be upregulated by ANG II. These encode the proteins for ferredoxin, Nor1, Nurr1, c6orf37, CAT-1, A20, MBLL, M-Ras, RhoB, GADD45alpha, and a novel protein designated FLJ45273.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375197

RAF2MgPmlaBGRORGs9vu1ZyDcW8ExUJ4XnT9ROkyydPoo
has assertion: p(EGID:183) -> r(HGNC:NR4A3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.955+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:183) -> r(HGNC:NR4A3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15375197

4
value: #------------------------------------------------------------------------------- Eleven genes were found to be upregulated by ANG II. These encode the proteins for ferredoxin, Nor1, Nurr1, c6orf37, CAT-1, A20, MBLL, M-Ras, RhoB, GADD45alpha, and a novel protein designated FLJ45273.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15375197

RAPcNUZdNIpqFEMJ6lxatFVwOP87Edx87k CMcB9HdJks
has assertion: tscript(p(HGNC:TP53)) -> cat(p(PFH:"CASP Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.962+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TP53)) -> cat(p(PFH:"CASP Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15377670

6
value: RNA interference and inducible gene expression approaches suggest that NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15377670

RAKcomFTh2GCDpgyYPIk1OLdr6TpXpvoIGGZq2DONFkgI
has assertion: p(HGNC:OSM) -> tscript(p(HGNC:STAT3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.963+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:OSM) -> tscript(p(HGNC:STAT3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15377837

5
value: Together these studies identify S100A9 as a novel OM-regulated gene through the STAT3-signaling cascade and suggest its involvement in the growth regulation of breast cancer cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15377837

RAJzLkzaGjCtJQF7LkFmdWtcdfj1P7vVvhH3Zt6 22R3U
has assertion: gtp(p(HGNC:RAC1)) -> tscript(p(PFH:"TCF/LEF Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.967+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(HGNC:RAC1)) -> tscript(p(PFH:"TCF/LEF Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15377999

6
value: Taken together, our data demonstrate a novel mechanism of Wnt pathway regulation whereby activation of Rac1 amplifies the signaling activity of stabilized/mutated beta-catenin by promoting its accumulation in the nucleus, and synergizing with beta-catenin to augment TCF/LEF-dependent gene transcription.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15377999

RAOTdEytM93uzRp1EyyVWwIolfKZOA-hffDJvwMUrfsjw
has assertion: p(HGNC:JUN,pmod(P,S,73)) => tscript(p(HGNC:JUN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.969+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:JUN,pmod(P,S,73)) => tscript(p(HGNC:JUN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15378002

5
value: VRK1 phosphorylates c-Jun in Ser63 and Ser73 in vitro, the same residues targeted by the N-terminal kinase of c-Jun (JNK). This phosphorylation induces the stabilization and accumulation of the c-Jun protein. VRK1 phosphorylates the endogenous c-Jun in Ser63. VRK1 activates c-Jun dependent transcription, which is dependent on phosphorylation of Ser63 and Ser73. The c-Jun with Ser63Ala and Ser73Ala substitutions is not transcriptionally active when cotransfected with VRK1. VRK1 interacts with c-Jun but not with JNK. The cotransfection of VRK1 and JNK has an additive effect on the transcriptional activation of c-Jun
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15378002

RAO8c2FRhy 9GshuyCBORTUCGcHk3Bvi1DDBIxLCDNWxI
has assertion: complex(p(MGI:Calcoco1),g(MGI:Ahr))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:27.993+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Calcoco1),g(MGI:Ahr))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15383530

3
value: We report here that CoCoA also binds the bHLH-PAS domains of AHR and ARNT and functions as a potent primary coactivator for them;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15383530

RAPwt5APpYa63UHic5kZMgiNOjTzR8gCx8fAp7R5OiNE8
has assertion: tscript(p(MGI:Trp53)) -> r(MGI:Mapk3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.003+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Trp53)) -> r(MGI:Mapk3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15383658

5
value: By contrast, serum- and glucocorticoid-inducible kinase 1 (SGK1) was significantly induced in a p53-dependent manner after DNA damage, and this induction was through extracellular signal-regulated kinase 1/2-mediated posttranslational regulation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15383658

RAHz6OjHDaWWw7BypuZuyyPg3zrXKZ8Zyye6rGF00cOw4
has assertion: tscript(p(HGNC:TLX1)) -> r(HGNC:SMARCD3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.009+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:TLX1)) -> r(HGNC:SMARCD3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15384172

5
value: We focused on examining genes found to be up-regulated according to the microarray analysis and selected three putative target genes, NFKB2, SMARCD3, and NR4A3, for further investigation. We could not only confirm the up-regulation of NR4A3 by an independent method in all clones expressing HOX11, but luciferase reporter assays demonstrated that the effect that HOX11 exerted on the proximal promoter of NR4A3 was dependent on the presence of an intact homeodomain, providing support for the idea that HOX11 manifests its regulatory function via its action as a transcription factor.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15384172

RAPR eIrJehaeILGIvIuFAzCGxPwiRGi9B z bf-CtSrI
has assertion: bp(GO:"response to hypoxia") -| bp(GO:"ATP synthesis coupled electron transport")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.017+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -| bp(GO:"ATP synthesis coupled electron transport")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15388515

2
value: Acute and 24-h hypoxia decreased JO2 of A549 cell mitochondrial complexes I, II, and III by 30-40%. Reoxygenation restored complex I activity after acute hypoxia but not after 24-h hypoxia. ATP was decreased 30% after 24-h hypoxia, but lactate production rate was not affected.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15388515

RAH9HzGqL097-LH9Td4yBAS96lDpcLEw8rX85S7xvXTnQ
has assertion: path(SDIS:"response to shear stress") -| r(HGNC:NOX4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.018+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"response to shear stress") -| r(HGNC:NOX4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15388638

3
value: Furthermore, OS increased gp91phox (nox2) and nox1 mRNA levels while decreasing nox4. In contrast, BMP4 induced nox1 mRNA expression, whereas nox2 and nox4 were decreased or not affected, respectively
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15388638

RANRk0I8zCAKVZNbfDdCWyItl7Jn2k1s64D6ZbytZmNbs
has assertion: p(HGNC:BMP4) -> a(CHEBI:"hydrogen peroxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.021+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:BMP4) -> a(CHEBI:"hydrogen peroxide")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15388638

3
value: Similar to OS, BMP4 stimulated H2O2 and O2- production in ECs.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15388638

RAE0A9ldGXORy0MP7lmJCn8qKu-eur2Lj7ba-2 iBrvDg
has assertion: p(HGNC:CLU) -| bp(GO:"response to oxidative stress")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.042+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CLU) -| bp(GO:"response to oxidative stress")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15389725

3
value: These findings suggest that clusterin may contribute to conferring resistance to oxidative stress-mediated cellular injury on prostate cancer cells, especially in the presence of androgen.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15389725

RAMEhyIJ3TiUcdAteedSHXf4OgpjAlsj2Wp UgTFhM3xw
has assertion: a(CHEBI:androgen) -> (p(HGNC:CLU) -| bp(GO:"response to oxidative stress"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.044+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:androgen) -> (p(HGNC:CLU) -| bp(GO:"response to oxidative stress"))
label: p(HGNC:CLU) -| bp(GO:"response to oxidative stress")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15389725

4
value: These findings suggest that clusterin may contribute to conferring resistance to oxidative stress-mediated cellular injury on prostate cancer cells, especially in the presence of androgen.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15389725

RAHNrn4WxMx7BJ3 HR6UD5l0sIefJ0xkEtQNc7snPE7DY
has assertion: cat(p(HGNC:PRDX6)) -| a(CHEBI:"hydrogen peroxide")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.050+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:PRDX6)) -| a(CHEBI:"hydrogen peroxide")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15448164

4
value: Finally, depletion of human Srx by RNA interference suggested that Srx is largely responsible for reduction of the Cys-SO2H of Prx in A549 human cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15448164

RANkz93QVWP rZmkNon8x-mAgXs0RsKzA8n5mUZdI-ql8
has assertion: p(HGNC:MAPK8,pmod(P)) => kin(p(HGNC:MAPK8))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.068+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:MAPK8,pmod(P)) => kin(p(HGNC:MAPK8))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15451030

5
value: These data indicate that in BMMC, Lyn contributes to SCF-induced phosphorylation of Kit, as well as phosphorylation of Jnks and Stat3.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15451030

RAPkl9xa-PZ0h10MzZpmy-krBI60AWmplBZJd3g4scmW8
has assertion: kin(p(HGNC:LYN)) -> tscript(p(HGNC:STAT3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.074+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:LYN)) -> tscript(p(HGNC:STAT3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15451030

6
value: These data indicate that in BMMC, Lyn contributes to SCF-induced phosphorylation of Kit, as well as phosphorylation of Jnks and Stat3.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15451030

RAN4HQu3YcdeZosaEdBRbylKrpihoAZR OcVnqpPSHXCM
has assertion: p(HGNC:HMOX1) -> tport(p(HGNC:SLCO2A1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.076+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:HMOX1) -> tport(p(HGNC:SLCO2A1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15451438

5
value: Endothelial cells expressing human HO-1 via retroviral transfer exhibit approximately 7-fold higher levels of PGT RNA and equivalently elevated uptake of [(3)H]PGE(2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15451438

RAFbp1JjcUtpMWwIEVTmX-GM x0k 2pmFiqAOu00sR7 o
has assertion: tport(p(HGNC:SLCO2A1)) -> a(SCHEM:Dinoprostone)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.077+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tport(p(HGNC:SLCO2A1)) -> a(SCHEM:Dinoprostone)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15451438

4
value: Endothelial cells expressing human HO-1 via retroviral transfer exhibit approximately 7-fold higher levels of PGT RNA and equivalently elevated uptake of [(3)H]PGE(2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15451438

RAIaO-6kjs5BwbItCiqrwb6UhosJgbIWGg3WN5JYRV-vA
has assertion: tscript(p(MGI:Foxa2)) -| r(MGI:Calca)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.088+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -| r(MGI:Calca)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: B: genes upregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAIjQdXvRmjCmwGfz-sUsa61GK5nMQV2hIB4TMDvhg6M0
has assertion: tscript(p(MGI:Foxa2)) -| r(MGI:Dlk1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.089+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -| r(MGI:Dlk1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: B: genes upregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAKvFJhkgQj0aVUD-Jj4TOC6pgfVcMR63eeJh00Zad9a0
has assertion: tscript(p(MGI:Foxa2)) -| r(MGI:Fabp5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.090+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -| r(MGI:Fabp5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: B: genes upregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAECygtfsE2X3BOi4Gk-KK9YdjR5vmttvo3m7Bpbnwxgk
has assertion: tscript(p(MGI:Foxa2)) -| r(MGI:Sftpb)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.106+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -| r(MGI:Sftpb)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: B: genes upregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAJ0fWx-9yUo4qCm-D2hXQgAUnJDlx4suk8k--N-GGmPo
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Atp2a2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.112+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Atp2a2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAFRkf4Oi8TvNmi4oP17QsmWLA4F7cXDOQ-2WTFwZIZcg
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:C3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.113+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:C3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RANWKK46GboBY3vg3ZO6IbWw0ETqTalzMaWLHFsMj2URE
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Foxa1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.117+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Foxa1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAL YEoxX9B6HLRSdqCzAJIWQVtAxYf 30q-8emt57a80
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Gstm5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.122+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Gstm5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAMTPQHEfUdWxcEdMI8ky8r-JCT8GOxeQROySUSUwDGL0
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Itga7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.124+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Itga7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAIhZV78GeheRrVa5rhkCdd1 tNuuhE aWq0ifafV45LQ
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Sfn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.146+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Sfn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAEh 949K1zwA8eZUCs4P0woeCw6aZ5v2p20F73L OiyA
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Tst)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.154+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Tst)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452354

5
value: table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452354

RAF2WAoEm2TO 5pfby4GLpqIbbVAwKQvatWoHQLH FQn4
has assertion: a(CHEBI:"trichostatin A") -> r(HGNC:BSG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.163+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"trichostatin A") -> r(HGNC:BSG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452378

3
value: The microarray analysis revealed that 8 genes including collagen type 1, alpha2 (COL1A2), insulin-like growth factor binding protein 2 (IGFBP2), integrin, alpha7 (ITGA7), basigin (BSG), quiescin Q6 (QSCN6), superoxide dismutase 3, extracellular (SOD3), nerve growth factor receptor (NGFR), and p53-induced protein (PIG11) exhibited substantial induction (ratio >2.0) after TSA treatment in multiple cell lines.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452378

RAOHW-X6zKycWY08aVjemQzM5XhpSPDassPwJ6qbrSENc
has assertion: a(CHEBI:"trichostatin A") -> r(HGNC:QSOX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.176+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"trichostatin A") -> r(HGNC:QSOX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452378

3
value: The microarray analysis revealed that 8 genes including collagen type 1, alpha2 (COL1A2), insulin-like growth factor binding protein 2 (IGFBP2), integrin, alpha7 (ITGA7), basigin (BSG), quiescin Q6 (QSCN6), superoxide dismutase 3, extracellular (SOD3), nerve growth factor receptor (NGFR), and p53-induced protein (PIG11) exhibited substantial induction (ratio >2.0) after TSA treatment in multiple cell lines.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452378

RAE71fWcgWpcSzMvKu34Hpjh4jXP5 CQQQ828rTgcrxJ4
has assertion: a(CHEBI:"trichostatin A") -> r(HGNC:SOD3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.177+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"trichostatin A") -> r(HGNC:SOD3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15452378

3
value: The microarray analysis revealed that 8 genes including collagen type 1, alpha2 (COL1A2), insulin-like growth factor binding protein 2 (IGFBP2), integrin, alpha7 (ITGA7), basigin (BSG), quiescin Q6 (QSCN6), superoxide dismutase 3, extracellular (SOD3), nerve growth factor receptor (NGFR), and p53-induced protein (PIG11) exhibited substantial induction (ratio >2.0) after TSA treatment in multiple cell lines.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15452378

Selventa

RANGIi7dRMM87MID6s90d8Xabrh3A26Sb1Lj-3HMjesnU
has assertion: a(CHEBI:"hydrogen peroxide") -| cat(p(PFH:"HDAC Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.183+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"hydrogen peroxide") -| cat(p(PFH:"HDAC Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15456740

4
value: H2O2 and CSC decrease HDAC activity and histone deacetylase 2 levels
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15456740

Selventa

RAIjYigm6adIcdNdSMcOEjay7FPql72w4vb1xrgJFcaBk
has assertion: p(HGNC:IL1B) -> tscript(p(HGNC:RELA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.185+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL1B) -> tscript(p(HGNC:RELA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15456740

5
value: Surprisingly, CSC (1, 2.5, and 5%) treatments did not cause any appreciable increase in NF-kB transactivation at 24 h in A549 cells. In preliminary studies, treatment of rat type II epithelial (L2) cells with CSC (1, 5, and 10%) for 4 h did not increase NF-kB DNA binding as assessed by electrophoretic mobility gel shift assay (data not shown) suggesting that CSC has no effect on NF-kB activation or transactivation in epithelial cells as revealed by various techniques. We also assessed the translocation of the p65 subunit of NF-?B from the cytoplasm to nucleus using the Cellomics Arrayscan technology. Using this technique, we showed increased nuclear p65 in response to IL-1b treatment (Fig. 7B), whereas CSC did not result in translocation of p65 from the cytoplasm to nucleus (data not shown).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15456740

Selventa

RAHRgOQHVSeZVByq3jgfhPulgOr8Ob1lIZdOOryMw2Dtk
has assertion: tscript(p(PFH:"NOTCH Family")) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.196+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(PFH:"NOTCH Family")) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15456857

4
value: Notch activation inhibits proliferation of endothelial cells in a cell-autonomous manner by inhibiting phosphorylation of the retinoblastoma protein (Rb)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15456857

Selventa

RAEYynIy55Yy UtbjbJt75OEeBasFF0wBh9eYLDQmO778
has assertion: p(HGNC:JAG1) => tscript(p(PFH:"NOTCH Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.199+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:JAG1) => tscript(p(PFH:"NOTCH Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15456857

5
value: we show that activation of the Notch pathway by the ligand Jagged1 reduces the proliferation of endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15456857

Selventa

RAN-T5Xafkj v107mu6-BbYuqj981OpQTNV vPn2jhd7s
has assertion: complex(p(HGNC:IRS1),p(HGNC:MDM2)) -> bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.206+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:IRS1),p(HGNC:MDM2)) -> bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15456867

5
value: In summary, we have found the following: (i) beta-arrestin-1 can alter insulin signaling by inhibiting insulin-induced proteasomal degradation of IRS-1; (ii) beta-arrestin-1 decreases the rate of ubiquitination of IRS-1 by competitively binding to endogenous Mdm2, an E3 ligase that can ubiquitinate IRS-1; (iii) dephosphorylation of S412 on beta-arrestin and the amino terminus of beta-arrestin-1 are required for this effect of beta-arrestin on IRS-1 degradation; and (iv) inhibition of beta-arrestin-1 leads to enhanced IRS-1 degradation and accentuated cellular insulin resistance.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15456867

Selventa

RAH9yqw5Vr8cGCnVeYfksnCEq55l1E3C2wZxsfaUcsNg0
has assertion: p(MGI:Cln5) -| r(MGI:Cbx1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.213+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Cbx1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAMjh7bqnzouYJZ08p7NGtYXT5r9HUHvyAS-oyeoFv0ak
has assertion: p(MGI:Cln5) -| r(MGI:Cxcl12)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Cxcl12)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAE5wfIcJ1Xawnrwzt4iEB2R4UGm8MpYvX1pdcGpHApaQ
has assertion: p(MGI:Cln5) -| r(MGI:Il4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.225+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Il4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAEB78OqaGYZUlH7jGIKebqjWaPdhKh2LuSbBg2tD6bAU
has assertion: p(MGI:Cln5) -| r(MGI:Nr4a2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.235+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Nr4a2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAKWKa5P74T4xUaKbc34xy6Olkf3NwKrC3wV4w2IRst6Q
has assertion: p(MGI:Cln5) -| r(MGI:Neurod6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.238+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Neurod6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAMKctNfB9LjYOYZza-x mvOMVNKTu-Vas-HEKw9Nnnfk
has assertion: p(MGI:Cln5) -| r(MGI:Nnat)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.239+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Nnat)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAEjhpjsiMJU2nz9323v4dKfAIYUrkRVxqFK3xHsF9wJI
has assertion: p(MGI:Cln5) -| r(MGI:Sncg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.248+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Sncg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAGqKWyxvpVi4k5xzgs N-qO0XId2a94yNSuZ GxAN1w4
has assertion: p(MGI:Cln5) -| r(MGI:Zfp40)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.255+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Zfp40)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAN4zZJ-EjGggI-0lcPSHGE8fjIjv43XTTIZpTDV2tfH8
has assertion: p(MGI:Cln5) -| r(MGI:Zfp54)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.256+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -| r(MGI:Zfp54)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RANGfCKZTZxLx8ahwPt0vxq6GuJIBWTNYND0 2dbXZYWo
has assertion: p(MGI:Cln5) -> r(MGI:C230052I12Rik)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.269+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(MGI:C230052I12Rik)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAFjPcPT4-wb9xyO06l-rStf1oPiM8VG9gexkwutXWDUQ
has assertion: p(MGI:Cln5) -> r(MGI:Cap1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.270+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(MGI:Cap1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAFkEFJHD1vTPvZsb8VQuU4UOAYgvwnOgVr IguGdyRag
has assertion: p(MGI:Cln5) -> r(MGI:Coch)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.271+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(MGI:Coch)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAIRSI1nW1A5eSGVfEReeFebUBURagH8fv-fpxXVSQ3j4
has assertion: p(MGI:Cln5) -> r(MGI:Myh7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.279+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(MGI:Myh7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAPjytvFdqk4CjrxvcU2Dc5SLWaElnNeuel74qt7Z2D68
has assertion: p(MGI:Cln5) -> r(EGID:57435)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.289+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(EGID:57435)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAPZez6Aa2imjUewYhIFqVLklzY6RBK1rXwprepqcUbxs
has assertion: p(MGI:Cln5) -> r(MGI:Slc4a5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.291+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Cln5) -> r(MGI:Slc4a5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15459177

4
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15459177

Selventa

RAG1KgD-JLQQCsn6sR87 ElIAOZWjWZNmgrN9IXTwdN2E
has assertion: p(HGNC:NINJ1) -| kin(p(HGNC:CDK2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.300+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NINJ1) -| kin(p(HGNC:CDK2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15464245

5
value: Ninjurin1-overexpressing clones exhibited strong growth inhibition due to G1 cell cycle arrest, which is associated with a posttranscriptional increase in p21WAF1/Cip1, a decrease of cyclin-dependent kinase 2 activity and the hypophosphorylation of Rb.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15464245

Selventa

RAGcVR-QLltd KFzVowkjrI2Tq0FF7uA1BjInQVUhaIYU
has assertion: kin(p(MGI:Kit)) -> kin(p(MGI:Mapk1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.318+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Kit)) -> kin(p(MGI:Mapk1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15465815

6
value: These data suggest that Spred-1 negatively regulates hematopoiesis by suppressing not only SCF-induced but also IL-3-induced ERK activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15465815

Selventa

RAF-RwWFWFp7WmDdPDTJ1jDfEW8OCJt2fMNcEVc7uCiX4
has assertion: kin(p(MGI:Kit)) -> kin(p(MGI:Mapk3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.320+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Kit)) -> kin(p(MGI:Mapk3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15465815

6
value: These data suggest that Spred-1 negatively regulates hematopoiesis by suppressing not only SCF-induced but also IL-3-induced ERK activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15465815

Selventa

RAMlr7oJ2EUudot1C4ii6UQd3ZKrDdu4q3fueVTiqSs3g
has assertion: a(SCHEM:Calcium) -> kin(p(PFR:"Camk2 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.366+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Calcium) -> kin(p(PFR:"Camk2 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15465923

4
value: We show that histamine synthesis stimulation by depolarization with 30 mM K(+) requires extracellular calcium entry, mostly through N-type channels, and subsequent activation of calcium/calmodulin-dependent protein kinase type II. In vitro, this kinase phosphorylated and activated histidine decarboxylase, the histamine-synthesizing enzyme.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15465923

Selventa

RAN00uChRU-hOPj3UBncW8U gwnWIqVzg1HZcwr196RAs
has assertion: cat(p(RGD:Hdc)) -> a(CHEBI:histamine)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.367+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(RGD:Hdc)) -> a(CHEBI:histamine)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15465923

4
value: We show that histamine synthesis stimulation by depolarization with 30 mM K(+) requires extracellular calcium entry, mostly through N-type channels, and subsequent activation of calcium/calmodulin-dependent protein kinase type II. In vitro, this kinase phosphorylated and activated histidine decarboxylase, the histamine-synthesizing enzyme.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15465923

Selventa

RAIYVQPJU4PG4sr1mp77A5aq96Nojzq2ntW u1RPcFpNw
has assertion: tscript(p(MGI:Pitx2)) => r(MGI:Nppa)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.378+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Pitx2)) => r(MGI:Nppa)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466416

5
value: Coexpression of MEF2A and PITX2a or Pitx2c resulted in a strong synergistic activation of the ANF promoter
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466416

Selventa

RANHWWvElrbsbd5aKMPreu4m2ohmeMTlYZNNEibQLYG8g
has assertion: cat(p(MGI:Cbs)) -> cat(p(MGI:Lcat))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.382+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Cbs)) -> cat(p(MGI:Lcat))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466479

6
value: the activity of lecithin-cholesterol acyltransferase was severely impaired in CBS(-/-) mice.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466479

Selventa

RAH08aGsErECI6SPqZUJH2Z8k2urKCCDRpyNpgW81NBZo
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Polr3k)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.384+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Polr3k)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: 104303_i_at 1500004O14Rik NM_025901 67005 EST
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAGeepN5h6FFGCVsoMiTO8kVYQY2Ev9P0cOGySHTweHxk
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Sema4b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.389+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Sema4b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: 95387_f_at Sema4b NM_013659 20352 semaphorin 4B
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAF9 2K3mKAsLX5 J2HZsuscVH55JDN1TMh2aVopOncSw
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Lpl)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.390+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Lpl)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: 95611_at Lpl NM_008509 16956 lipoprotein lipase
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAEGKxMZHzi8r0KsOVbphykTmyqBMX91uZi33LkInS-L0
has assertion: a(SCHEM:Tretinoin) -> r(MGI:2810025M15Rik)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.393+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:2810025M15Rik)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: ESTs 97374_at 2810025M15Rik NM_027274 69953 RIKEN cDNA 2810025M15 gene
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RALKMTTmjvopYcY4k bs n8CTirp-8ZJ2HYvM-cZ1AeMU
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Tbca)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.394+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Tbca)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Other 93333_at Tbca NM_009321 21371 tubulin cofactor a
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAGf2TD1EPkRvgeHuSH-1E5L9rhqjF0ayAuKSB8FElaMw
has assertion: a(SCHEM:Tretinoin) -| r(MGI:Csnk1d)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.412+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -| r(MGI:Csnk1d)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 2. Group 1: Genes downregulated by RA at 6 h
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAPZx0m8wL7sXCVgHgrjXJ87Xaq0-OUIfn5kBwvZS8tOc
has assertion: a(SCHEM:Tretinoin) -| r(MGI:Pros1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.420+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -| r(MGI:Pros1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 2. Group 1: Genes downregulated by RA at 6 h
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RALAyQgCEduZGLMMN5i5MeNuBQve0OH-MaTFZdOnVDTXc
has assertion: a(SCHEM:Tretinoin) -| r(MGI:Ubn1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.422+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -| r(MGI:Ubn1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 2. Group 1: Genes downregulated by RA at 6 h
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAOGS9G7riCrbynfFakm1oGruNvQmXkpWeT leswHm7Gc
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Igf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.431+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Igf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 3. Group 2: Genes induced by RA at all times
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAI-6tMv U0U-t6pCMJpFv8-1G--SPp8XZF34SD oiw1c
has assertion: a(SCHEM:Tretinoin) -| r(MGI:Itm2a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.439+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -| r(MGI:Itm2a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 4. Group 3: Genes suppressed by RA
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAPS96X85Ry2UpYkySXg9WrAcBHn07lE8k0JDjIdCc2pc
has assertion: a(SCHEM:Tretinoin) -| r(MGI:Nov)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.441+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -| r(MGI:Nov)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Table 4. Group 3: Genes suppressed by RA
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAHCUWgfMY0pV8vRW7t2NEx1RAs4jifQDa vMViJXWUb8
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Hoxd4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.444+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Hoxd4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Transcription factor 102380_s_at Hoxd4 NM_010469 15436 HoxD4
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAI8ovXr6jjugdmzBOsnEUEwNn1rJdb7KF57Wszah-eHA
has assertion: a(SCHEM:Tretinoin) -> r(MGI:Fabp5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.445+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Tretinoin) -> r(MGI:Fabp5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466718

3
value: Transport 160544_at Fabp5 NM_010634 16592 mal1; Mus musculus Fabpe gene
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466718

Selventa

RAKS XxKkoyq5xUAcKiNQNzT0SP0EXyCn551u465WRL-k
has assertion: kin(p(HGNC:PRKCZ)) -> complex(p(HGNC:UBE4B),p(HGNC:FEZ1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.448+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKCZ)) -> complex(p(HGNC:UBE4B),p(HGNC:FEZ1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15466860

7
value: Interaction between E4B and FEZ1 in mammalian cells was enhanced by coexpression of constitutively active PKCzeta.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15466860

Selventa

RAEVe2A66lzVfePWRrdvGhzkjdTW5zqqEIO4laDTjrDEU
has assertion: p(HGNC:NRG1) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.474+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NRG1) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467735

3
value: proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467735

Selventa

RAPJpoW8NVeSad5K-HM-Qs7FNpw27LxuqdMlgpXHc4PPA
has assertion: p(HGNC:NRG1) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.477+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NRG1) -> bp(GO:"cell proliferation")
label: tscript(p(HGNC:HES1)) -> (p(HGNC:NRG1) -> bp(GO:"cell proliferation"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467735

6
value: proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467735

Selventa

RAOOMAKRksclHxBkSy23yAfxaJxRz2YTUOf9fYI ZmHSo
has assertion: kin(p(HGNC:AKT1)) -> p(HGNC:GSK3A,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.485+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) -> p(HGNC:GSK3A,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467756

5
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467756

Selventa

RAFEvm7KqLecVWJlc oT20SBJEbTTC25N9lfK0ExCU ZU
has assertion: kin(p(HGNC:AKT1)) -> tscript(p(HGNC:RELA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.487+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:AKT1)) -> tscript(p(HGNC:RELA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467756

6
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467756

Selventa

RAFkB5q77VHF0LmBHIVfy6AD1K6PB q8mL9BGQFtcNCQs
has assertion: bp(GO:"DNA methylation") -| r(HGNC:HAND1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.501+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"DNA methylation") -| r(HGNC:HAND1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467763

3
value: Treatment of a cancer cell line with a demethylating agent, 5-aza-2'-deoxycytidine, restored the expression of 13 genes, RASGRF2, ADAM23, NEF3, NKX2-8, HAND1, EGR4, PRG2, FBN2, CDH2, TLL1, NPTX1, NTSR1 and THBD, showing their silencing by methylation of their 5' CGIs.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467763

Selventa

RAKXNKRzzfo1osqOvWQ5w2Qn4Ya-1bdTStj65vz927kvg
has assertion: bp(GO:"DNA methylation") -| r(HGNC:NPTX1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.504+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"DNA methylation") -| r(HGNC:NPTX1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15467763

3
value: Treatment of a cancer cell line with a demethylating agent, 5-aza-2'-deoxycytidine, restored the expression of 13 genes, RASGRF2, ADAM23, NEF3, NKX2-8, HAND1, EGR4, PRG2, FBN2, CDH2, TLL1, NPTX1, NTSR1 and THBD, showing their silencing by methylation of their 5' CGIs.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15467763

Selventa

RALDxFpWLspzoqF1zd7b1JHzxF1sBJkQdh2WvZMtMPP04
has assertion: p(PFH:"TGFB Family") -> r(HGNC:TIMP3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.514+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFH:"TGFB Family") -> r(HGNC:TIMP3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15468069

4
value: activation of ERK-MAPK pathway and Sp1 transcription factor play a pivotal role in the induction of TIMP-3 by TGF-beta in chondrocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15468069

Selventa

RAP95giGdsw Po2zOzB1Gktm0F6iRMrB7CPZhLg0woSsw
has assertion: cat(p(HGNC:SIRT1)) -| p(PFH:"Histone H3 Family",pmod(M,K,79))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.521+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SIRT1)) -| p(PFH:"Histone H3 Family",pmod(M,K,79))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15469825

5
value: Gal4-SirT1 expression resulted in the deacetylation of H4-K16 and H3-K9, recruitment of H1 within the promoter vicinity, drastically reduced reporter expression, and loss of H3-K79 methylation, a mark restricting silenced chromatin...recruitment and deacetylation of histone H1,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15469825

Selventa

RAP vntw2Tz6O3WAxO8B L3yj0XlgYkin8czZl4kPWiUA
has assertion: cat(p(HGNC:SMPD1)) -> a(CHEBI:ceramide)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.522+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SMPD1)) -> a(CHEBI:ceramide)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15469904

4
value: Ceramide, the hydrolysis product of sphingomyelin, seems to be a key mediator as it mimics mmLDL by inducing activation of the same signaling components
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15469904

Selventa

RAIlejJ6jfUbdT2u23uDkFtafONTG9cgrSSYkElXg7M9w
has assertion: a(SCHEM:"Oxidized Low Density Lipoprotein") -> cat(p(HGNC:SMPD2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.526+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Oxidized Low Density Lipoprotein") -> cat(p(HGNC:SMPD2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15469904

4
value: minimally modified LDL (mmLDL) mainly activated components involved in stress response and apoptotic cell death including p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase/stress-activated protein kinase (JNK) as well as neutral and acid sphingomyelinase
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15469904

Selventa

RAKE2KCb7CXHUL1K8WhPPD23PrdE8wQ7kA9a-b5GiQ zU
has assertion: a(CHEBI:androgen) -> r(HGNC:AR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.546+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:androgen) -> r(HGNC:AR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15472231

3
value: Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15472231

Selventa

RAE4bb9S6QPVB0mx6n-PKAh9pLCiczYuNulphoiMKRniw
has assertion: bp(GO:"response to hypoxia") -> p(HGNC:HIF1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.549+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> p(HGNC:HIF1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15474002

3
value: In order to investigate the mechanisms of hypoxic regulation of PFKFB4 gene expression, we used dimethyloxalylglycine, which has the ability to mimic effect of hypoxia by significant induction of hypoxia-inducible factor (HIF-1alpha) protein levels.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15474002

Selventa

RAHXjGPUdfhAM9aOCnNLk78vah5yktvGH9jCUHMgi8xNE
has assertion: cat(p(HGNC:EIF2S1)) -> p(HGNC:INS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.551+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:EIF2S1)) -> p(HGNC:INS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475356

5
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475356

Selventa

RAO N-9watT-Fri08vNV73 3LZbl5pEjhTE9 dDmMkk0Q
has assertion: a(CHEBI:gefitinib) -| r(HGNC:ARF5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.553+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:ARF5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RANFCYNst5E79i8r2PpWQDhQ8UnCCNlOO1cscDtCWKXzY
has assertion: a(CHEBI:gefitinib) -| r(HGNC:CCNC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.557+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:CCNC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAMJdQD1 uec9XX wB MFg0nhVYok6ggO6Elvln2l3KIU
has assertion: a(CHEBI:gefitinib) -| r(HGNC:SMARCA5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.595+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:SMARCA5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAPsxTfUtzng9-abI-l12HWm3mnlhXvQYMsNzNYJYvZWE
has assertion: a(CHEBI:gefitinib) -| r(HGNC:STEAP2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.597+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:STEAP2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAGFAaDIEPqPPxkZVbqc-qi0e3RzosI17jAUN9iFHQHzY
has assertion: a(CHEBI:gefitinib) -| r(HGNC:TUSC3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.602+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:TUSC3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RANwHvABjeDVTG7j2k5jQK-SSYcSJ3epDJ0k71zucRPjI
has assertion: a(CHEBI:gefitinib) -| r(HGNC:TBCE)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.603+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:TBCE)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAH19nuOwr-xPFDP0IzdHEwrCzc0iAD60JfIX5BGqcoUc
has assertion: a(CHEBI:gefitinib) -| r(HGNC:TOP2A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.605+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:TOP2A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAL3bQf8KbS3zcyXpB9mrTJi2k1nQZLAs49L-lVbc0Fww
has assertion: a(CHEBI:gefitinib) -| r(HGNC:ZFP37)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.611+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -| r(HGNC:ZFP37)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAHC5YTTEkiz0fZNXJVZ1cmXcgtgp8azq4bC33s56X8ek
has assertion: a(CHEBI:gefitinib) -> r(HGNC:BST2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.615+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -> r(HGNC:BST2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAIYEHxObKjAKWqV-2YcZdxxF0trFojsqy3DAuSdoqkdw
has assertion: a(CHEBI:gefitinib) -> r(HGNC:CTSD)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.617+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -> r(HGNC:CTSD)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAH9bieljk1KuMpGqGifmooXu5oFn0b3KHzZEST2NcdAo
has assertion: a(CHEBI:gefitinib) -> r(HGNC:IGFBP3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.625+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:gefitinib) -> r(HGNC:IGFBP3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475436

3
value: See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475436

Selventa

RAGZRT64jyUz47SETr8vQKz7oCmy78-wgyRlJzx8Eot08
has assertion: a(SCHEM:PHA665752) -| p(HGNC:HGF)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.642+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:PHA665752) -| p(HGNC:HGF)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15475459

3
value: PHA-665752 effectively blocked the biological responses to HGF in all assays, with 50% inhibition at 5 to 15 nmol/L concentration and complete inhibition at around 100 nmol/L.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15475459

Selventa

RAN43Lvx9pW9oTXv oZxnA6xunKJaXM83CIU4fU-5g-xU
has assertion: a(SCHEM:"smoke condensate, cigarette (particulate phase)") -> p(RGD:Cxcl1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.646+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"smoke condensate, cigarette (particulate phase)") -> p(RGD:Cxcl1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15477004

3
value: The mean CINC-1 concentration was higher in PPexposed animals compared with gas phase-and shamexposed animals (Table 1). Interestingly, gas phaseexposed animals had a lower mean CINC-1 concentration compared with sham animals ( p = .005, Table 1).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15477004

Selventa

RAMxWHfJQw20Gc3QGAGZiHXDcM6UczGllpj-mTjrw3ses
has assertion: path(SDIS:"viral infection") -| r(HGNC:GSN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.654+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"viral infection") -| r(HGNC:GSN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15479839

3
value: TABLE 2. Statistically significant cytoskeleton-, extracellular matrix-, and adhesion-related genes consistently upmodulated (positive fold change) or downmodulated (negative fold change) across late times of infection [in response to CMV infection]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15479839

Selventa

RAG188kTxbuwvf4LCkMBu0yTJvXEi-40MOhya9PTmsxZo
has assertion: p(HGNC:TXN) -> tscript(complex(NCH:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.665+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TXN) -> tscript(complex(NCH:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15480426

4
value: Trx facilitates the transcriptional activities of nuclear factor NFkB and the glucocorticoidrecept or via direct associations with their DNA-binding domains (Matthews et al., 1992; Hayashi et al., 1993; Qin et al., 1995; Makino et al., 1999).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15480426

Selventa

RALsxC1OluHLaH9t US14Sf68a2qkoSpUavnTpDRxYMYk
has assertion: kin(p(HGNC:ATM)) -> p(PFH:"PRKAA Family",pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.672+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ATM)) -> p(PFH:"PRKAA Family",pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15485651

5
value: Immunoprecipitates of ATM collected from IGF-1-stimulated cells also caused the phosphorylation of the AMPK-alpha subunit in vitro.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15485651

Selventa

RAOMy2lz8Yumey-2O-s0AkqMOaIxD5DrIv9AJyXzlpH2w
has assertion: complex(p(MGI:Npm1),p(MGI:Cdkn2a)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.683+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Npm1),p(MGI:Cdkn2a)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15485902

5
value: NPM is released from ARF-containing protein complexes, and in vivo S phase progression ensues.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15485902

Selventa

RAP9mXK J0j-Li3YznlV5zPbcv2WOqv7h0WKZAtWqkNUI
has assertion: kin(p(HGNC:RAF1)) => p(HGNC:RB1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.692+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:RAF1)) => p(HGNC:RB1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15485920

5
value: Disruption of the Rb-Raf-1 interaction by a nine-amino-acid peptide inhibits Rb phosphorylation, cell proliferation, and vascular endothelial growth factor-mediated capillary tubule formation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15485920

Selventa

RAN9P1atsywEt eFPdPYQaU6f2zGw-LZWIzP6e08pGQSg
has assertion: tscript(p(HGNC:KLF6)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.696+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:KLF6)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15486921

4
value: Functionally, wild-type KLF6 decreased cellular proliferation of HepG2 cells, while patient-derived mutants did not.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15486921

Selventa

RAHa3rdGuaMJbnJJy1OK7T2bFjgU3bAUXZlkMPNg3QvEE
has assertion: bp(GO:aging) -| r(HGNC:ISLR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.697+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:ISLR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15489060

3
value: 31 genes were confirmed to be up- or down-regulated during replicative senescence by semi-quantitative RT-PCR. The overexpressions of several genes including CD36, putative lymphocyte G0/G1 switch gene (G0S2), tumor protein D52-like 1 (TPD52L1), chemokine (C-X-C motif) ligand 6, myxovirus resistant gene 1 (MX1), and the down-regulation of the immunoglobulin superfamily containing leucine-rich repeat (ISLR), neurotrimin, insulin-like growth factor 2 associated protein (IGF2A), and apoptosis-related RNA binding protein (NAPOR3) were newly identified.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15489060

Selventa

RAMXNMsNkI-LZMkMz9JcbKMfWB1WCxHiLpt2rJzS-dNWQ
has assertion: p(HGNC:TNF) -> tscript(complex(NCH:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.712+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/15489375

4
value: TNF-? stimulated NF-?B-dependent promoter activity (Fig. 5D), that rottlerin had little effect on TNF-?-induced NF-?B-dependent promoter activity, and that PDTC diminished NF-?B-dependent promoter activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15489375

Selventa

RAJy1WnOn3cgZ02Gh5IFFEhR-82UWBCpMrn Hnk01bYoA
has assertion: p(HGNC:TNF) -> p(HGNC:NFKBIA,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.714+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TNF) -> p(HGNC:NFKBIA,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15489375

4
value: TNF-alpha induced both phosphorylation and degradation of IKappaB-alpha in A549 cells within several minutes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15489375

Selventa

RAFv9pwyzDD4FIpcKTN7SDrGILjj7OYJdOwYv1dBHu8wA
has assertion: p(HGNC:ID1) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:ID1) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15489884

3
value: ectopic expression of Id1, but not Id2, allowed continued proliferation of immortalized mammary epithelial cells and breast cancer cells. Conversely, downregulation of Id1 impaired proliferation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15489884

Selventa

RANCq3JfLHikfsONjkR3i2idgj-YMUmnHWCsCgZSYJzLM
has assertion: p(HGNC:PRKCH) -> p(EGID:2475)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.726+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PRKCH) -> p(EGID:2475)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15489897

4
value: Stimulation of PKCs in U-251 cells for 30 min with 100 nM PMA, showed an increased phosphorylation of mTOR at ser-2448 by 43+/-10-fold compared with untreated cells. Expression of PKC-etaKR, a kinase dead mutant of PKCeta significantly reduced PMA stimulated ser-2448 phosphorylation of mTOR by 54+/-12%. In U-1242 PKCdeltaNPS, a catalytically active PKC expression increased phosphorylation on ser-2448 of mTOR by 322+/-58% as compared to the empty vector, suggesting that PKCeta activates mTOR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15489897

Selventa

RAI2LK09mdS39gIr6cO-NEJ vu-tSYnN0M7zv5QGxmt9Q
has assertion: complex(p(HGNC:YWHAZ),p(HGNC:CTNNB1)) => tscript(p(HGNC:CTNNB1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.729+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:YWHAZ),p(HGNC:CTNNB1)) => tscript(p(HGNC:CTNNB1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492215

7
value: 14-3-3zeta Interacts with beta-Catenin and Activates beta-Catenin-Dependent Promoters in HEK293T cells and Colon Carcinoma cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492215

Selventa

RAMWqsU4vlHVl8pp3lSRawbvfdgmOjbOJrP1s7pfJdM4A
has assertion: gtp(p(PFM:"Ras Family")) -> r(MGI:Alkbh3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.735+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFM:"Ras Family")) -> r(MGI:Alkbh3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

5
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAMw4TtseIgpTYR4HK4uUCeWlTcSVXhz4lkE8Zo98148w
has assertion: gtp(p(PFM:"Ras Family")) -> r(MGI:Col18a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.739+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFM:"Ras Family")) -> r(MGI:Col18a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

5
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAKI1HSciEYSEqiPn08xqO-N2066P72AOwvNGUL8-sm3c
has assertion: gtp(p(PFM:"Ras Family")) -> r(MGI:Crisp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.742+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFM:"Ras Family")) -> r(MGI:Crisp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

5
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAFlLueUm2IJf3zSzjrkHzTMHCc-Diqe5F6T7Oxz9liDg
has assertion: gtp(p(PFM:"Ras Family")) -> r(MGI:Sox5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.759+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFM:"Ras Family")) -> r(MGI:Sox5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

5
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAO1mecxcaQrS14mfFXRRvzSfd4ybWEFYdWD9ZP3dL54Q
has assertion: gtp(p(PFM:"Ras Family")) -> r(MGI:Tslp)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.763+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFM:"Ras Family")) -> r(MGI:Tslp)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

5
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAF6Cvf4S-oBomNcMCLPFsLmAZAkC925XZ9otMsmarx08
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Crisp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.770+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Crisp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

4
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAGp7JTbxZ-Kv3A9S0WDVawx-VPGGnOu46rRc83VKvP98
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Klf3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.772+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Klf3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

4
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAInA4wbkmYMoN8D4Y-EeER33kaJthNWG-yiJ4O1Hs4Qc
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rnf19b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.781+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Rnf19b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

4
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAIYqTqB-1KdK69-GrJSfre7FHdlaO2FAwF5RZxH-ftMs
has assertion: tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Sh3rf1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.784+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"Nfkb Complex")) -> r(MGI:Sh3rf1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492243

4
value: Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492243

Selventa

RAJXSi1wO52rbDRGSqE4f-4BdmbYCSQ3r5 ISne1YBmDU
has assertion: kin(p(HGNC:MAPK3)) -> tscript(p(HGNC:ETS1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.791+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) -> tscript(p(HGNC:ETS1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492268

6
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492268

Selventa

RAI8oz6t0efw9VFgilv8jd9GKewL Zhwk9CvR76oQkP3E
has assertion: cat(p(HGNC:AKR1C1)) -| a(CHEBI:progesterone)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.832+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AKR1C1)) -| a(CHEBI:progesterone)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492289

4
value: Suppression of ARK1C1 and AKR1C2 by selective small interfering RNAs inhibited production of 20alpha-dihydroprogesterone and was associated with increased progesterone in MCF-10A cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492289

Selventa

RAH7k0UPXBPlMMQSzRmnb4vEXTWN3V3r8zAMJpdP-2Tio
has assertion: cat(p(HGNC:AKR1C2)) -| a(CHEBI:progesterone)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.833+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AKR1C2)) -| a(CHEBI:progesterone)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492289

4
value: Suppression of ARK1C1 and AKR1C2 by selective small interfering RNAs inhibited production of 20alpha-dihydroprogesterone and was associated with increased progesterone in MCF-10A cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492289

Selventa

RAEz639q4aVPyJgG7TRKpGNaV0C92rxMdSe4Mt8kr6Hos
has assertion: cat(p(HGNC:RNF43)) -> bp(GO:"cell growth")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.837+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:RNF43)) -> bp(GO:"cell growth")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15492824

4
value: Its exogenous expression conferred a growth-promoting effect in COS7 and NIH3T3 cells, and suppression of its expression by specific short interfering RNAs retarded the growth of colon cancer cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15492824

Selventa

RAPIb5Qjr9uS JvA6Uzo4tMdjUBbty9LQuFA73F LsSwY
has assertion: p(HGNC:FZD2) -> a(SCHEM:Calcium)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.840+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FZD2) -> a(SCHEM:Calcium)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15494017

3
value: The Wnt/Ca(2+)/cGMP pathway mediated by Frizzled-2 was discovered recently. Activation of this pathway leads to increased intracellular concentrations of Ca(2+) and decreased intracellular concentrations of cGMP. On the basis of results from these three analyses, the cGMP-specific phosphodiesterase, PDE6, is demonstrated to be an effector for the Wnt/Ca(2+)/cGMP signalling pathway of development, which is mediated by Frizzled-2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15494017

Selventa

RAJYiHg8duJp5u1GEOf5FBTHf97J lw1bysL152jvwNfQ
has assertion: p(HGNC:SMAD3,pmod(P)) => tscript(p(HGNC:SMAD3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.845+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SMAD3,pmod(P)) => tscript(p(HGNC:SMAD3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15494412

5
value: TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, was also suppressed by VEGF. VEGF attenuation of TGF-beta action was also demonstrated in two other endothelial cell lines. In conclusion, VEGF attenuates TGF-beta action in the human endothelial cell, specifically at the level of transcription of PAI-1 gene and Smad2/3 phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15494412

Selventa

RAOPAHi8G9nDlL6bisPhWO6VtGDv2U G4vtNxcWIrYtEo
has assertion: p(HGNC:TGFB1) -> p(HGNC:SMAD2,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.847+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFB1) -> p(HGNC:SMAD2,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15494412

4
value: TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, was also suppressed by VEGF. VEGF attenuation of TGF-beta action was also demonstrated in two other endothelial cell lines. In conclusion, VEGF attenuates TGF-beta action in the human endothelial cell, specifically at the level of transcription of PAI-1 gene and Smad2/3 phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15494412

Selventa

RAJ5pM4aBt17DoGE7VAWgrXaKsgy0rZorfKxLeTeDHkxg
has assertion: p(MGI:Igbp1) -| tscript(p(MGI:Trp53))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.871+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Igbp1) -| tscript(p(MGI:Trp53))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15499020

5
value: As a result of alpha4 deletion, multiple proapoptotic genes were transcribed.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15499020

Selventa

RAO4ha7Xw8emG49tZN6jHUJl0YvPx93Rn8S9JEnT94sQw
has assertion: p(HGNC:PTK2B,pmod(P,Y)) -> kin(p(PFH:"MAPK Erk1/3 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.872+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PTK2B,pmod(P,Y)) -> kin(p(PFH:"MAPK Erk1/3 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15499613

5
value: Our data show that in a glioma-derived cell line the cytoplasmic tyrosine kinase PYK2 is constitutively associated with HER3 and that stimulation with Heregulin results in PYK2 tyrosine phosphorylation. HER3, but not HER2, mediates the phosphorylation of the C-terminal region of PYK2 to promote a mitogenic response through activation of the MAPK pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15499613

Selventa

RAPuE yigiHpGmTv49njmBXgKTJ9GDN8MDCh3sXY6lOQc
has assertion: a(SCHEM:"serum leptin") -| r(RGD:Car3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.875+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"serum leptin") -| r(RGD:Car3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15500001

3
value: leptin decreased CA III expression while insulin increased it which suggests that the decrease in CA III expression observed in obesity in rat adipose tissue may be related to hyperleptinemia.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15500001

Selventa

RAIDTNisi FUintnYTamxES9Yw3xEiY5yqAUT3eWaASWw
has assertion: kin(p(HGNC:SRC)) => p(HGNC:SRC,pmod(P,Y,530))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.884+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:SRC)) => p(HGNC:SRC,pmod(P,Y,530))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15504335

5
value: The chief phosphorylation sites of Src include tyrosine 416 that results in activation from autophosphorylation and tyrosine 527 that results in inhibition from phosphorylation by C-terminal Src kinase
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15504335

Selventa

RAK2-REWkq3bmSYVWDGPC7TfL-NhXZnTXDjS1QYs-Z7dQ
has assertion: a(SCHEM:Lithium) -| r(HGNC:IMPA2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.886+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Lithium) -| r(HGNC:IMPA2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15504365

3
value: IMPA2 promoter activity in both cell lines is downregulated, in a dose-dependent manner, by lithium
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15504365

Selventa

RAGDEWKxUK CBAM8hRaO49fldEPt 9o6YfpIv1ai5ASGo
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> r(HGNC:EN1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.894+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> r(HGNC:EN1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15504738

4
value: Five DNA replication and repair-related genes (FEN1, PCNA, RFC4, TOP2A, and TYMS) were suppressed by LY294002 treatment as detected by real time PCR (Fig. 6C).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15504738

Selventa

RAF8QGjf5qHoSmWstRghSA1y3RNF6Ce5ggoGE52vo8Ufc
has assertion: kin(p(PFH:"AKT Family")) -> r(HGNC:TYMS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.911+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"AKT Family")) -> r(HGNC:TYMS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15504738

5
value: The expression of active mAKT1 blocked the down-regulation of CKS2, HEC, UBE2C, and ZWINT genes (cell cycle-related, Fig. 7B); of RFC4 and TYMS genes (DNA replication and repair-related, Fig. 7B); and of HMGB2 and HIST1H4C genes (chromatin-related, Fig. 7, B and C) induced by the anti-HER2 antibody.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15504738

Selventa

RAPt7qYb k2WiJiYUD9a5qYptJlVnXLH1mIfN3AdC0X g
has assertion: kin(p(PFH:"AKT Family")) -> r(HGNC:ZWINT)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.914+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"AKT Family")) -> r(HGNC:ZWINT)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15504738

5
value: The expression of active mAKT1 blocked the down-regulation of CKS2, HEC, UBE2C, and ZWINT genes (cell cycle-related, Fig. 7B); of RFC4 and TYMS genes (DNA replication and repair-related, Fig. 7B); and of HMGB2 and HIST1H4C genes (chromatin-related, Fig. 7, B and C) induced by the anti-HER2 antibody.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15504738

Selventa

RAKK0k7LI52037VXDOnVC-aXkXDk2NticpXeRz2sY89aA
has assertion: kin(p(PFM:"Prka Family")) -> p(MGI:Tnni3,pmod(P,S,24))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.923+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFM:"Prka Family")) -> p(MGI:Tnni3,pmod(P,S,24))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15507454

5
value: Within the cardiac isoform's amino-terminal extension, serines are present at residues 23 and 24 (Ser23/Ser24), which serve as substrates for protein kinase A (PKA), which is activated in response to ?-adrenergic stimulation of the heart (3). Several investigations report that PKA-mediated phosphorylation of cTnI results in a reduction in myofilament Ca2+ sensitivity (4), an increase in cross-bridge cycling (5), and increased binding of cTnI to the thin filament. Cardiac TnI is also a substrate for protein kinase C (PKC) phosphorylation at Ser43/Ser45 and Thr144 (position 143 in the human protein) (6). However, the substrate specificity of these sites is not absolute, since PKC can phosphorylate the PKA sites (7-9).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15507454

Selventa

RALze5SinZCZnOG7EFbpvgC6m0foJ5qGVb2u15yroDqUY
has assertion: r(MGI:Il6) -> p(MGI:Il6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.935+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

r(MGI:Il6) -> p(MGI:Il6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15507530

4
value: results indicate that BCL-6 negatively regulates proliferation of the monocytic/macrophage lineage by suppressing an autocrine IL-6/STAT3-mediated gene expression program.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15507530

Selventa

RAI5jYEzG80xdVBumfk-CxOMk1FLkY0sjS2S3FLKsmZZ4
has assertion: tscript(p(MGI:Bcl6)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.937+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Bcl6)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15507530

4
value: results indicate that BCL-6 negatively regulates proliferation of the monocytic/macrophage lineage by suppressing an autocrine IL-6/STAT3-mediated gene expression program.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15507530

Selventa

RAMHMgmbxOs41pgZ7SSVSdeE8le6pdx-DOQX RCq38g-M
has assertion: a(SCHEM:"Adenosine triphosphate") -| kin(complex(NCH:"AMP Activated Protein Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.958+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Adenosine triphosphate") -| kin(complex(NCH:"AMP Activated Protein Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

3
value: AMPK is therefore activated by any stress that depletes cellular ATP
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RAFjXlCmA1Ke31K6rPS46LXx7PM6QUz73pfPMixuszXBo
has assertion: p(HGNC:EP300,pmod(P,S,89)) =| cat(p(HGNC:EP300))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.959+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:EP300,pmod(P,S,89)) =| cat(p(HGNC:EP300))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

5
value: Finally, it (AMPK) phosphorylates the ubiquitous co-activator p300 at a specific site (Ser89), reducing its ability to bind to nuclear hormone receptors and thus activate their target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RANt1MDh2Uy3Ci-947FaY2BuEX Drq9yHyJtmHraTeELI
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| cat(p(HGNC:EP300))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.962+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:EP300))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

5
value: Finally, it (AMPK) phosphorylates the ubiquitous co-activator p300 at a specific site (Ser89), reducing its ability to bind to nuclear hormone receptors and thus activate their target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RANKd1Pn Awy36U0e0qGX9eFSgkJb 24hJyoWIPfM9axk
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -> p(HGNC:EP300,pmod(P,S,89))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.963+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")) -> p(HGNC:EP300,pmod(P,S,89))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

4
value: Finally, it (AMPK) phosphorylates the ubiquitous co-activator p300 at a specific site (Ser89), reducing its ability to bind to nuclear hormone receptors and thus activate their target genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RALYmva-HoJCMT5ttkFIR9QTD7c2nd1gmmnZrss73xAaE
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| cat(p(HGNC:GYS1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.973+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:GYS1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

5
value: the mechanism for AMPK activation by stresses involves an upstream kinase... The upstream kinase purified from rat liver is a complex between LKB1, STRAD and MO25 and all three subunits are required for full activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RAKd3-akOekrr5SYIPtyDEk0NStbNT7ranNIvqZf21 CY
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| cat(p(HGNC:PCK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.976+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:PCK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15509864

5
value: the mechanism for AMPK activation by stresses involves an upstream kinase... The upstream kinase purified from rat liver is a complex between LKB1, STRAD and MO25 and all three subunits are required for full activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15509864

Selventa

RAN4Ifjt yXG0-vhXuWhhZtqni-j8VGbeMHi281VKUx7g
has assertion: kin(p(MGI:Ntrk1)) -> p(MGI:Rasgrf1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.985+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Ntrk1)) -> p(MGI:Rasgrf1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15513915

5
value: Previously, we demonstrated a novel interaction between the intracellular domain of the nerve growth factor-regulated TrkA receptor tyrosine kinase and an N-terminal fragment of RasGrf1. We now show that RasGrf1 is phosphorylated and interacts with TrkA, -B, and -C in co-transfection studies.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15513915

Selventa

RAJfXjmbUTZnFlM1kBlH0sCmUjpCrQHy7EjBeP0Zg AHc
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:AHCYL1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.993+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:AHCYL1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RAJIdelZdf88YtwqEfMy Ep r0ZSFmF1XiFMlXB0vElpY
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:AHCYL1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.994+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:AHCYL1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RAM2ONhLJu46igkx0mJXG5VTXQn4Ues4mhz0HiXEgiHTw
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:B4GALT1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.997+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:B4GALT1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RAPEQ6LWqLqEAdADSKV6YyskqyjD1Gudb9Q3shVmuzGzM
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:BRCA1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:28.998+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:BRCA1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RAI-gVArhFWfQb3I-AKZb78g8BLN59xnlr61v9Yc2r5zI
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:PRKAR1A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.010+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:PRKAR1A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RAP5cDnDloz8f0gm8Fl0IqmIeClbvpgEmY5COpnSD9WpU
has assertion: composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:PRSS23)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.011+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

composite(a(CHEBI:estradiol),complex(NCH:"AP-1 Complex")) -> r(HGNC:PRSS23)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514030

4
value: Table 2. Estrogen-Induced/AP-1-Dependent Genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514030

Selventa

RALyQf-NA9hjvJYzoz9hoj7xxRT3jgP0o9bxBnIXZB3UQ
has assertion: p(RGD:Adcyap1) => cat(p(RGD:Adcyap1r1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.016+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Adcyap1) => cat(p(RGD:Adcyap1r1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514088

5
value: Their actions have been shown to be mediated by three different receptor subtypes: PAC1-R, which has exclusive affinity for PACAP, and VPAC1-R and VPAC2-R, which have equal affinity for PACAP and VIP.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514088

Selventa

RAKcB0D3-OnXIKqm9wcugLvklmi64RFRZ9T7dHH4c3o3w
has assertion: cat(p(HGNC:AGTR1)) -> p(HGNC:TGFB1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.022+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:AGTR1)) -> p(HGNC:TGFB1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514164

5
value: Collagen synthesis is activated via the angiotensin II type 1 (AT1) receptor. We demonstrate that transforming growth factor-beta1, a major product of stimulated AT1 receptor, does not activate solely collagen synthesis but synergistically the synthesis of hnRNP A1, E1, and K as well.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514164

Selventa

RALlSaOhh4JIuSNoU9hvQZgYdrC9w7Jm1nweR0tHyeDMc
has assertion: p(HGNC:HNRNPA1) => r(HGNC:COL1A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.025+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:HNRNPA1) => r(HGNC:COL1A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514164

4
value: Reporter gene cell transfection experiments and RNA stability assays show that hnRNPs A1, E1, and K stimulate collagen expression by stabilizing mRNAs We report identification of three mRNA-binding proteins, heterogeneous nuclear ribonucleoprote (hnRNP) A1, E1, and K, as positive effectors of collagen synthesis acting at the post-transcriptional level by interaction with the 3'-untranslated regions (3'-UTRs) of COL1A1, 1A2, and 3A1 mRNAs
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514164

Selventa

RAJwtHo2528i0L5tUAg00qQJcm26oMdKl15SpzFe9yRCk
has assertion: p(HGNC:HNRNPK) => r(HGNC:COL1A2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.027+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:HNRNPK) => r(HGNC:COL1A2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514164

4
value: Reporter gene cell transfection experiments and RNA stability assays show that hnRNPs A1, E1, and K stimulate collagen expression by stabilizing mRNAs We report identification of three mRNA-binding proteins, heterogeneous nuclear ribonucleoprote (hnRNP) A1, E1, and K, as positive effectors of collagen synthesis acting at the post-transcriptional level by interaction with the 3'-untranslated regions (3'-UTRs) of COL1A1, 1A2, and 3A1 mRNAs
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514164

Selventa

RAMxd5RhbmunfEOu6TX-jYqUKThuUm-UxZU8GMaBnKJBU
has assertion: p(HGNC:HNRNPK) => r(HGNC:COL1A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.029+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:HNRNPK) => r(HGNC:COL1A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514164

4
value: Reporter gene cell transfection experiments and RNA stability assays show that hnRNPs A1, E1, and K stimulate collagen expression by stabilizing mRNAs We report identification of three mRNA-binding proteins, heterogeneous nuclear ribonucleoprote (hnRNP) A1, E1, and K, as positive effectors of collagen synthesis acting at the post-transcriptional level by interaction with the 3'-untranslated regions (3'-UTRs) of COL1A1, 1A2, and 3A1 mRNAs
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514164

Selventa

RAJeV1u F5WlKWr64uYv1oR4AGcBaSJXt7xvAA0 ydhCg
has assertion: path(SDIS:"food intake") -| r(MGI:Mtx2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.035+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"food intake") -| r(MGI:Mtx2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15514260

3
value: Table 4. Gene ontology biological process groupings for differentially expressed genes in FR (food restriction) mice
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15514260

Selventa

RALkpjDl1kahC6ojiTaOX4lAlFQB0NBOBUjjk6fZ1mXzM
has assertion: tscript(p(HGNC:SMAD1)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.040+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:SMAD1)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15516492

4
value: Furthermore, p38(MAPK), ERK1/2, JNK, and Smad1 were phosphorylated by BMP4. Using specific MAPK inhibitors, a dominant negative Smad1 construct, and Smad1 siRNA, we found that the antiproliferative and prodifferentiation effects of BMP4 were Smad1 dependent with JNK also contributing to differentiation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15516492

Selventa

RAFl1toim8Qtq53HR0H7Gu6q8y17FPyZtROY88Un0yN-c
has assertion: p(HGNC:DKK3) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.046+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:DKK3) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15516983

3
value: Ectopic expression of Dkk-3/REIC in HeLa, Hep3B and Huh 7 cells led to suppression of cell growth, which was primarily attributable to induction of cell apoptosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15516983

Selventa

RAIeY sxzxSYkuEzzNrEKEx8BkE m1VIX00QTc5r Cpr4
has assertion: a(SCHEM:"Thioctic acid") -> a(CHEBI:glutathione)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.054+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Thioctic acid") -> a(CHEBI:glutathione)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15519889

2
value: LA pretreatment maintains the intracellular level of reduced glutathione
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15519889

Selventa

RAEUFnpWgJ6OQh1Xgb8n2d0135Zc3uQvTWuRvmZE-uTV8
has assertion: tscript(p(HGNC:PPARD)) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.066+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:PPARD)) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15519889

4
value: activation of PPARd is associated with an anti-obesity and more insulin sensitive phenotype
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15519889

Selventa

RAOsMQ ILs2cxBWkT9qkjA3xGJN9WYjuoCj6yae5hSuaw
has assertion: tscript(p(HGNC:PPARD)) -| bp(MESHPP:Obesity)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.067+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:PPARD)) -| bp(MESHPP:Obesity)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15519889

4
value: activation of PPARd is associated with an anti-obesity and more insulin sensitive phenotype
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15519889

Selventa

RAMyHam2ELmYonX2lw5pjeipzl3i7NxMT8S6-HuffMbXI
has assertion: kin(complex(NCH:"AMP Activated Protein Kinase Complex")) -| bp(MESHPP:"Insulin Resistance")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.070+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")) -| bp(MESHPP:"Insulin Resistance")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15519889

3
value: adiponectin and leptin contribute to an insulin-sensitive phenotype via their ability to activate AMP-activated kinase and increase fatty acid oxidation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15519889

Selventa

RAGhlfcuGABE1Xryhv70kIHZnpmHvj30lZ BzPe6MF4xI
has assertion: a(CHEBI:ceramide) -| kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.073+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:ceramide) -| kin(p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15519889

4
value: ceramide, diacylglyceride and long chain acyl-coenzyme A esters can also suppress the insulin signaling pathway, as reported for the ceramide induced inhibition of protein kinase B phosphorylation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15519889

Selventa

RAPBQGndFOYizMhFXF9WF96DQovSXiRKQ14azbS3QZKbk
has assertion: p(HGNC:SMAD2,pmod(P)) => tscript(p(HGNC:SMAD2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.084+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SMAD2,pmod(P)) => tscript(p(HGNC:SMAD2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15520171

5
value: Western blotting revealed higher expression of phosphorylated SMAD2 in wt-ACVR2 transfectants versus controls, suggesting cells deficient in ACVR2 had impaired SMAD signaling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15520171

Selventa

RAF3XOe7HpRus7Ln7r6OsFNMjMr97p bjNbNCB1-ytN0s
has assertion: kin(p(HGNC:ACVR2A)) -> tscript(p(HGNC:SMAD2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.087+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ACVR2A)) -> tscript(p(HGNC:SMAD2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15520171

6
value: Western blotting revealed higher expression of phosphorylated SMAD2 in wt-ACVR2 transfectants versus controls, suggesting cells deficient in ACVR2 had impaired SMAD signaling.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15520171

Selventa

RANZyKmgDGvh5m6hZWr4OQLAPlwd1EpGA PTO325z7gD0
has assertion: a(CHEBI:progesterone) -| path(SDIS:"invasive cancer")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.088+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:progesterone) -| path(SDIS:"invasive cancer")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15520195

2
value: % Boyden chamber invasion assay revealed that PR-transfected MDA-MB231 cells also lost most of their invasive properties after Pg treatment.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15520195

Selventa

RAEQOaaJ9XyItrpXuPqKiRPNYnJ3GMSDh4RgRO9z9hJ9M
has assertion: a(CHEBI:rosiglitazone) -> r(MGI:Cox7a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.097+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:rosiglitazone) -> r(MGI:Cox7a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15520860

3
value: Table 1 Rosiglitazone-induced mitochondrial gene expression in ob/ob mouse adipocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15520860

Selventa

RAG-uSA hxanlgiSxpH2EioialwyGVEwRorF0gyRkn8G0
has assertion: a(CHEBI:rosiglitazone) -> r(MGI:Cox8b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.101+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:rosiglitazone) -> r(MGI:Cox8b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15520860

3
value: Table 1 Rosiglitazone-induced mitochondrial gene expression in ob/ob mouse adipocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15520860

Selventa

RAP5u1r2GpXCS9NbM7G9fQQlg9M7Bjtdlzwva53JwclXY
has assertion: p(MGI:Csf3) -> bp(GO:"neutrophil differentiation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.123+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Csf3) -> bp(GO:"neutrophil differentiation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15522959

3
value: G-CSF-induced differentiation was accompanied by up-regulation of genes associated with neutrophil differentiation, including gp91pHOX and matrix metalloproteinase (MMP9; gelatinase b), whereas expression of macrophage scavenger receptor 2 (MSR2), a marker of monocytic differentiation, was down-regulated.39,45 Conversely, M-CSF-induced differentiation was accompanied by up-regulation of MSR2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15522959

Selventa

RAORMj2FHmA1jTCPnZiguFoIFkc-zkqxeT9B9CanwFPnE
has assertion: cat(p(HGNC:TGFBR2)) -> tscript(p(HGNC:SMAD3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.126+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:TGFBR2)) -> tscript(p(HGNC:SMAD3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15522964

6
value: Furthermore, acute and long-term pretreatment of ECs with thrombin or PAR1 peptide agonist suppressed the TGF-beta-induced serine phosphorylation of Smad2, a critical mediator of TGF-beta signaling. Moreover, activation of PAR1 led to a profound and spread cytosolic clustering formation of Smad2/3 and markedly prevented Smad2/3 nuclear translocation evoked by TGF-beta1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15522964

Selventa

RAHrVLv-16uVoJM4GfU1Q-CuRCGR7eQExtFyfGQ9YpAbw
has assertion: a(SCHEM:Stanolone) -| r(MGI:Car3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.135+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Car3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAEGl85vQI1OMFrCn2SkWqYR-6gepBJ5g7 Gc2xrZL76s
has assertion: a(SCHEM:Stanolone) -| r(MGI:Car3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.136+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Car3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAObLa9R1q6HLTe1nheM1LXQUYQefLICNTTG-UWIRR0gQ
has assertion: a(SCHEM:Stanolone) -| r(MGI:Cst6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.141+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Cst6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAGtogpX1H91CEdk4v3jRnLUjGYFGT46AUnvT5Bf8ouAg
has assertion: a(SCHEM:Stanolone) -| r(MGI:Ctnnb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.146+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Ctnnb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAMLTDzf-AW2lTb3yQ49O8axo0S Fl-uzEUJvA0Y3vKQE
has assertion: a(SCHEM:Stanolone) -| r(MGI:Hsp90aa1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.158+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Hsp90aa1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAOBM4 rwwzd5w7iUivpqlFYdv8rAuap31KjMdwoGiO-A
has assertion: a(SCHEM:Stanolone) -| r(MGI:Itgb1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.160+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Itgb1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAN vosHNVt92 5jy2d4LwQdWaHbemXnJzSJxAuIu2k-8
has assertion: a(SCHEM:Stanolone) -| r(MGI:Krt1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.163+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Krt1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAIH0zs0pkI3k6hwBCVxG8QJt5eGSwUMkw-sZTo58pRug
has assertion: a(SCHEM:Stanolone) -| r(MGI:Krt5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.166+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Krt5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAKJXn1bqky7b2FKdfGsHSN6-wBSoqc4FCMAP3U3ykc4Q
has assertion: a(SCHEM:Stanolone) -| r(MGI:Mgll)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.172+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Mgll)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAJ9uH30cJe6yNnYyxjeOSVbKlAcWMHDNikXL2cTdu3ow
has assertion: a(SCHEM:Stanolone) -| r(MGI:Rplp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.183+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Rplp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAPpFJEiUT4 bKQefKDy0K7p55IHlC3H7ineFYrgFy6C8
has assertion: a(SCHEM:Stanolone) -| r(MGI:Sepp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.189+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Sepp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAJIN8-YDJCJA3fy9H9p9v 4pU-zRwhhaLDw-jVivJ-mI
has assertion: a(SCHEM:Stanolone) -| r(MGI:Tnni2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -| r(MGI:Tnni2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAMZDe3NNsD6pr9oYQW5-lLZmm5cI7zAMYz8WZcX4pZWo
has assertion: a(SCHEM:Stanolone) -> r(MGI:Acsl1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.210+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Acsl1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAMbbLkEa35V8JjFHlbX9InafRK1vm8wjre-90RDyn2XY
has assertion: a(SCHEM:Stanolone) -> r(MGI:Atp5o)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.214+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Atp5o)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAIZ5k-JV1z-uWpc9vGwYYJ-3y0HCy7ZhHHex-4zOpyGY
has assertion: a(SCHEM:Stanolone) -> r(MGI:Cdo1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.227+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Cdo1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAIadDNLk FkYAUOdrtHWkS59RTgIttiJbGf7D3tKUtw8
has assertion: a(SCHEM:Stanolone) -> r(MGI:Col5a3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.231+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Col5a3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RANP7oDEGxzwtEYohrD442j-84MocJpRAXY5ZSAERiD9M
has assertion: a(SCHEM:Stanolone) -> r(MGI:Ephx2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.242+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Ephx2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAOzA82sokX6j6-ZvI26uY0EDYxPd-ZE5L8A5g0pbRrFY
has assertion: a(SCHEM:Stanolone) -> r(MGI:Elovl6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.243+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Elovl6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAPuNpP0pvg YOOG5xlEow4XvPM6niY5dR2VS7SSCEmhU
has assertion: a(SCHEM:Stanolone) -> r(MGI:Glrx3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.252+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Glrx3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAG1Ap6DANhYu9bHmRMpDv1sTKMCTLT0NLff9l3W9Taqw
has assertion: a(SCHEM:Stanolone) -> r(MGI:Gpd1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.254+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Gpd1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAK1c6c7FXbveNnR6EF0snfgMd-UT9cvP6GDeyxtak0nI
has assertion: a(SCHEM:Stanolone) -> r(EGID:384422)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.264+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(EGID:384422)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAI-tO WiycKXFHKEYbr47VGdWfzeia ErOiM7IKNnUdg
has assertion: a(SCHEM:Stanolone) -> r(MGI:Laptm4a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.267+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Laptm4a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAMXBYUDmvnL2DihobFlH8-zAHzG2L7hdXdfbUwa9VipQ
has assertion: a(SCHEM:Stanolone) -> r(MGI:Lpl)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.308+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Lpl)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAEM2fbZO0cH4Qf2k8KtXsFFYB13tP1DAbTWnuVT7Eje4
has assertion: a(SCHEM:Stanolone) -> r(MGI:Mup2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.316+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Mup2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAO88iXxVwo myRQRkBM3y0OG2pHcmypDGJjCk0-HuNSo
has assertion: a(SCHEM:Stanolone) -> r(MGI:Pcnt)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.322+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Pcnt)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAGTSwuhYFs462Fh0xhQiG2KBgxkS3uM SPZlnkGRxDEE
has assertion: a(SCHEM:Stanolone) -> r(MGI:Pck1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.326+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Pck1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RANQHT-ESTxKDMm76qtqR-cd8 HXzB7OTlejZ4wSBaxK8
has assertion: a(SCHEM:Stanolone) -> r(MGI:Pcx)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.327+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Pcx)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAOCdlF8qmM3uFG4Tx8iHL-TRH6YuvjEApdddZhK7sYeg
has assertion: a(SCHEM:Stanolone) -> r(MGI:Sparc)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.343+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Sparc)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAP3lzcnoPStcmZ3Pplzvn3E7tYOVp7akwvfyJqUILYnE
has assertion: a(SCHEM:Stanolone) -> r(MGI:Sqstm1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.348+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Sqstm1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAOHdYJQSpEnEyxd0JRip5PewPOiZ9I948ad4G8bLBtvQ
has assertion: a(SCHEM:Stanolone) -> r(MGI:Tkt)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.352+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Tkt)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAGtIwWso5N7vCBD AkDJMdM7WNzjsui8Od-U1cb5BPGE
has assertion: a(SCHEM:Stanolone) -> r(MGI:Ubc)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.360+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Ubc)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAPvIh6Oj8itwmvvO2KBGoX68X63Fwmngo6Tci8TToa20
has assertion: a(SCHEM:Stanolone) -> p(EGID:633082)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.364+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> p(EGID:633082)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: Tables 2-8 - effects of dihydrotestosterone on gene expression in adipose tissue
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RANL7qs3NvuLMV6MhEFbxlTTl29xyy1ddxahGVB2TCohI
has assertion: a(SCHEM:Stanolone) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.366+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

2
value: The present results provide global genomic evidence for a stimulation of glycolysis, fatty acids and triacylglycerol production, lipolysis and cell shape reorganization, as well as cell proliferation and differentiation, by DHT.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAId2TFgFiZMLBw4Sdw28xvURyVm9qEhYnMjpgBqJl55Q
has assertion: a(SCHEM:Stanolone) -> r(MGI:Col1a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.376+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Col1a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: transcripts involved in adipogenesis, and cell cycle and cell shape organization, such as DDX5, C/EBPalpha, cyclin I, procollagen types I, III, IV, V and VI, SPARC and matrix metalloproteinase 2, were upregulated by DHT.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RANEGhi8Wv3L3INkBuLoTA04eJOlV1veZYyZEhuDgymFA
has assertion: a(SCHEM:Stanolone) -> r(MGI:Col3a1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.378+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Col3a1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: transcripts involved in adipogenesis, and cell cycle and cell shape organization, such as DDX5, C/EBPalpha, cyclin I, procollagen types I, III, IV, V and VI, SPARC and matrix metalloproteinase 2, were upregulated by DHT.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAK1TlYC0DHG-SfHbJAFgKLcLPNBjEOV55W 8oneAIjfU
has assertion: a(SCHEM:Stanolone) -> r(MGI:Mmp2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.382+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Stanolone) -> r(MGI:Mmp2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15525599

3
value: transcripts involved in adipogenesis, and cell cycle and cell shape organization, such as DDX5, C/EBPalpha, cyclin I, procollagen types I, III, IV, V and VI, SPARC and matrix metalloproteinase 2, were upregulated by DHT.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15525599

Selventa

RAH5ZB4QaXXWYaEwbh8IfMveJ6pR-Yu--rKe0TODtD oY
has assertion: p(HGNC:KIT,pmod(P,Y,721)) -> kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.391+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:KIT,pmod(P,Y,721)) -> kin(p(PFH:"AKT Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526160

5
value: Activation of PI3-kinase by c-Kit has been linked to mitogenesis, differentiation, survival, adhesion, secretion and actin cytoskeletal reorganization . In c-Kit, Y721 has been found to directly interact with PI3-kinase [82]. c-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526160

Selventa

RAKDYuIQbH9fjDFJCTwVPlTRk9DUE2bpAxV4cwtCT0Dx0
has assertion: kin(p(HGNC:KIT)) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.394+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:KIT)) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526160

4
value: Activation of PI3-kinase by c-Kit has been linked to mitogenesis, differentiation, survival, adhesion, secretion and actin cytoskeletal reorganization . In c-Kit, Y721 has been found to directly interact with PI3-kinase [82]. c-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526160

Selventa

RAE9Y8DM5COTjPYJYY9M2FPLhJjV-ccAGgM7YlOw3-zdk
has assertion: complex(p(HGNC:KIT),p(HGNC:KIT)) => kin(p(HGNC:KIT))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.404+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:KIT),p(HGNC:KIT)) => kin(p(HGNC:KIT))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526160

7
value: The c-Kit ligand SCF is expressed as a glycosylated transmembrane protein. Binding of SCF to c-Kit results in dimerization of the receptors followed by activation of its intrinsic tyrosine kinase activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526160

Selventa

RAKk2CgZbipmXtfQCa3ZBwLEijj7rdba 3DAuBLq9t8CQ
has assertion: phos(p(HGNC:PTPN6)) -| kin(p(HGNC:KIT))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.407+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(HGNC:PTPN6)) -| kin(p(HGNC:KIT))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526160

6
value: The protein tyrosine phosphatase SHP-1 interacts with Y570 of c-Kit and negatively regulates c-Kit signaling
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526160

Selventa

RANRCgGH3PrxgtO8-4xsO-M3tX0u7wxLlQbQBbfQ2foGM
has assertion: cat(complex(p(HGNC:ITGA2),p(HGNC:ITGB1))) -> bp(GO:phagocytosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.411+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(complex(p(HGNC:ITGA2),p(HGNC:ITGB1))) -> bp(GO:phagocytosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526166

6
value: Other functions associated with Fc receptor-mediated phagocytosis, such as the activation of NADPH-oxidase, were not affected in Gsn-/- mice [55]. An impairment of complement- opsonized phagocytosis was observed in capG/Gsn double-null mice, providing evidence for distinctive and non-overlapping functions of capG and gelsolin in phagocytic processes [50]. Finally, binding and internalization of collagen beads, a process dependent on a2 b1 integrin [53], was also shown to be affected in Gsn-/- fibroblasts [56].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526166

Selventa

RAM0cFI9TFTyPMQguA3tQdsIwIOkj91gjB-kOs4z3ymrI
has assertion: a(SCHEM:Calcium) => cat(p(HGNC:GSN))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.413+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Calcium) => cat(p(HGNC:GSN))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15526166

4
value: Recently, a third isoform (gelsolin-3) has been described [9]. Gelsolin-3 is cytoplasmic and is characterized by 11 additional residues at the N-terminus. Gelsolin-3 is expressed in oligodendrocytes and mainly in the brain, lungs and testis [9], but its specific function is still unknown. Gelsolin contains six gelsolin-like (G) domains and was first described as a protein able to bind and sever actin filaments, and to control polymerization of barbed ends. Furthermore, this protein also initiates formation of actin filaments by binding two monomeric actin molecules. Gelsolin activity is regulated by Ca2+, intracellular pH, phosphoinositides and tyrosine phosphorylation. Crystallographic studies of gelsolin complexed with its substrate have been recently performed [10-14]. Results have been reviewed in [15] and will not be discussed here. The other gelsolin superfamily members; villin, advillin, supervillin and flightless, have additional domains beyond the sixfold repeat. Villin has been demonstrated to participate in cytoskeleton remodeling in response to various stimuli in the intestine [16]. Flightless is the only member of gelsolin superfamily that has been shown to be essential for mouse development [17]. Among all of the proteins forming the gelsolin superfamily, adseverin (also named scinderin) is the one that shares the highest degree of homology with gelsolin. Indeed, adseverin shares 60% amino acid homology with gelsolin [18], and displays Ca2+-regulated actin filament severing activity. As compared to gelsolin, adseverin has a more restricted expression. Adseverin was first discovered in platelets, megakaryocytes and chromaffin cells [19]. This protein is present in all secretory cells and is involved in actin cytoskeleton remodeling occurring during exocytosis [19-22]. With flightless [23] and supervillin [24, 25], capG (also named gCap39, Mbh1 or macrophage capping protein) is the only other protein of gelsolin family sharing a nuclear localization [26,[cell cut: 3464 characters, first 2000 kept]
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15526166

Selventa

RAG4OP-KUTz2mnzLaRSbs0aGTcgpYYu6XWxYhF5mTDMYE
has assertion: tscript(p(HGNC:SREBF2)) -| tscript(p(HGNC:SMAD3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.419+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:SREBF2)) -| tscript(p(HGNC:SMAD3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15527767

6
value: Interactions of AGP7, sex-determining region Y protein, actin beta and sterol regulatory element binding protein-2 (SREBP-2) proteins with Smad3 constructs were confirmed by immunoblotting with specific antibodies. Interaction of Smad3 with SREBP-2 was also confirmed by co-immunoprecipitation of myc-Smad3 and Flag-SREBP-2 upon expression in mammalian cells. We found that SREBP-2 inhibited the transcriptional activity of Smad3 in luciferase reporter assays
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15527767

Selventa

RAJP6AmtQA-z2Ub6dnGINBOYehgXBStmzXSEOdFVWiI1k
has assertion: bp(GO:"macrophage activation") -| r(HGNC:IL1RN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.425+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"macrophage activation") -| r(HGNC:IL1RN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15528358

3
value: \"Differential gene expression modulated by the cytoplasmic domain of Fc gamma RIa (CD64) alpha-chain.\" Expression of M-CSF, MIC-1, and LSP1 was greater after stimulation of WT-Fc{gamma}RI relative to the TL-Fc{gamma}RI, while expression of MIP-2 and IL-1Ra were lower after stimulation of WT-Fc{gamma}RI relative to the TL-Fc{gamma}RI (Table II).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15528358

Selventa

RAEbZWtI15PCpal9x NsXWjuBfY-kjIiaDVgWIR0sW4qE
has assertion: cat(p(PFH:"CD64 Family")) -> r(HGNC:GDF15)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.433+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(PFH:"CD64 Family")) -> r(HGNC:GDF15)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15528358

5
value: \"Differential gene expression modulated by the cytoplasmic domain of Fc gamma RIa (CD64) alpha-chain.\" Expression of M-CSF, MIC-1, and LSP1 was greater after stimulation of WT-Fc{gamma}RI relative to the TL-Fc{gamma}RI, while expression of MIP-2 and IL-1Ra were lower after stimulation of WT-Fc{gamma}RI relative to the TL-Fc{gamma}RI (Table II).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15528358

Selventa

RAKfu3h97HnGbjiYp9FeQJDGsa6UjOnlm bJL3bM9wFtQ
has assertion: a(SCHEM:Hydrocortisone) -> r(HGNC:CXCR4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.436+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Hydrocortisone) -> r(HGNC:CXCR4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15528395

3
value: Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15528395

Selventa

RAHYFI3b9YSxuWxu3CpIBAYG3KBHRixYrvt22GZU8n23Y
has assertion: path(SDIS:Diabetes) positiveCorrelation a(SCHEM:"3-Nitrotyrosine")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.441+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:Diabetes) positiveCorrelation a(SCHEM:"3-Nitrotyrosine")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15531508

2
value: Moreover, because metformin has protective effects on nondiabetic beta-cells exposed to high glucose or free fatty acid levels, we investigated its direct action on T2D islet cells. Diabetic islets were characterized by reduced insulin content, decreased amount of mature insulin granules, impaired glucose-induced insulin secretion, reduced insulin mRNA expression, and increased apoptosis with enhanced caspase-3 and -8 activity. These alterations were associated with increased oxidative stress, as shown by higher nitrotyrosine concentrations, increased expression of protein kinase C-beta2 and nicotinamide adenine dinucleotide phosphate reduced-oxidase,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15531508

Selventa

RAP4zy6RQRoWsKDEQ1Kwsk5VLJ8431eqWVl6MVqWjBObw
has assertion: a(CHEBI:metformin) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.446+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:metformin) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15531508

2
value: Twenty-four-hour incubation of T2D islets with metformin was associated with increased insulin content, increased number and density of mature insulin granules, improved glucose-induced insulin release, and increased insulin mRNA expression. Moreover, apoptosis was reduced, with concomitant decrease of caspase-3 and -8 activity. These changes were accompanied by reduction or normalization of several markers of oxidative stress. Thus, T2D islets have several functional and survival defects, which can be ameliorated by metformin; the beneficial effects of the drug are mediated, at least in part, by a reduction of oxidative stress.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15531508

Selventa

RALBLGO1WmmDVknvbm53hIvsGSqGO0SI6-oO3zppI qk0
has assertion: a(CHEBI:metformin) -> r(HGNC:INS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.449+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:metformin) -> r(HGNC:INS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15531508

3
value: Twenty-four-hour incubation of T2D islets with metformin was associated with increased insulin content, increased number and density of mature insulin granules, improved glucose-induced insulin release, and increased insulin mRNA expression. Moreover, apoptosis was reduced, with concomitant decrease of caspase-3 and -8 activity. These changes were accompanied by reduction or normalization of several markers of oxidative stress. Thus, T2D islets have several functional and survival defects, which can be ameliorated by metformin; the beneficial effects of the drug are mediated, at least in part, by a reduction of oxidative stress.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15531508

Selventa

RAEHHHntanTnHq85QAEUzwh6aIG1hUr8dv3ZNzJ2FCE1Q
has assertion: p(HGNC:IL6) -> p(HGNC:STAT3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.459+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IL6) -> p(HGNC:STAT3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15535835

4
value: IL6 induces phosphorylation of STAT3 on Tyr705 and activates STAT3.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15535835

Selventa

RAKyAhP1FiSoyMUhg1hvtsm0t92Rha0gxPxHyK0 9hVV0
has assertion: p(MGI:Nfkbia) -| tscript(p(MGI:Hes1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.470+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Nfkbia) -| tscript(p(MGI:Hes1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15536134

5
value: TNF-alpha treatment results in a temporary release of IkappaBalpha from the hes1 promoter that correlates with increased histone acetylation and transcriptional activation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15536134

Selventa

RAEOwm-YhyGWdnqSYuFS-L9zzGC6u ChPrL-33u43EIc8
has assertion: tscript(p(MGI:"Nkx2-5")) -> r(MGI:Gja5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.475+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:"Nkx2-5")) -> r(MGI:Gja5)
label: tscript(p(MGI:Tbx5)) -| (tscript(p(MGI:"Nkx2-5")) -> r(MGI:Gja5))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15537493

8
value: Furthermore, co-transfection experiments showed the ability of Nkx2-5 and GATA4 to transactivate the minimal Cx40 promoter while Tbx5 repressed Nkx2-5/GATA4-mediated activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15537493

Selventa

RAPLh063v1JB-u5PxDGkw61Oq6BkdEHdCVnogNi0P4MVA
has assertion: cat(p(HGNC:FTH1)) -| a(CHEBI:"reactive oxygen species")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.483+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/15537542

4
value: FHC is induced downstream of NF-kappaB and is required to prevent sustained JNK activation and, thereby, apoptosis triggered by TNFalpha. FHC-mediated inhibition of JNK signaling depends on suppressing ROS accumulation and is achieved through iron sequestration.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15537542

Selventa

RANfGI4u7IK enEX-e539FUZvToDOyxb7J uB-kYtjR0M
has assertion: a(CHEBI:testosterone) -> r(MGI:Arg2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.498+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:testosterone) -> r(MGI:Arg2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15539552

3
value: pharmacological doses of testosterone simultaneously down-regulated the level of OAT protein and up-regulated the expression of arginase II and ODC genes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15539552

Selventa

RAOQJSjqXLWiQa0SaEZ1kIA60ibslwMBkTYbr8B0WLuMQ
has assertion: complex(p(HGNC:ERBB3),p(HGNC:ERBB2)) -> cat(p(HGNC:ERBB3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.511+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:ERBB3),p(HGNC:ERBB2)) -> cat(p(HGNC:ERBB3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542435

7
value: Additional genetic and pharmacologic experiments show that this modulation of AR function is mediated by the HER2/ERBB3 pathway, not by EGFR.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542435

Selventa

RANUzGiMdIz1Bse1gvumFL8VeqTcwbCfgJXbp7N-97mqo
has assertion: cat(p(HGNC:ERBB3)) -> p(HGNC:AR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.515+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:ERBB3)) -> p(HGNC:AR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542435

5
value: This HER2/ERBB3 signal stabilizes AR protein levels and optimizes binding of AR to promoter/enhancer regions of androgen-regulated genes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542435

Selventa

RAJRKdYys8MxuMc98MmoXeNDu8c-3bc45svFLWbpNAyno
has assertion: p(RGD:Il6) -| p(RGD:Rps6ka1,pmod(P))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.520+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(RGD:Il6) -| p(RGD:Rps6ka1,pmod(P))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542570

4
value: IL-6 infusion resulted in muscle atrophy characterized by a preferential loss of myofibrillar protein (-17%). IL-6 induced a decrease in the phosphorylation of ribosomal S6 kinase (-60%) and STAT5 (-33%), whereas that of STAT3 was increased approximately twofold.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542570

Selventa

RALLU9fEw47cL-nEm7 ohoFq3fA522TRC3HCO3DHjWg30
has assertion: a(CHEBI:histamine) -> a(SCHEM:Calcium)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.540+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:histamine) -> a(SCHEM:Calcium)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542600

2
value: A GRK2-specific small interfering RNA effectively reduced GRK2 expression and resulted in a significant increase in histamine-promoted calcium flux.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542600

Selventa

RAKmrN9H7uum folAUNnAl91AQRSKQKr8ucu7VfusdZzw
has assertion: p(HGNC:VRK1) -> bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.550+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:VRK1) -> bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542844

3
value: Suppression of VRK1 expression by specific small interfering RNA provokes several defects in proliferation, situating the protein in the regulation of this process.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542844

Selventa

RAKO8bvfn3XjjKkqSPG69OqvEcR0lNAhf6XGkhz2ISBKc
has assertion: p(MGI:Gata6) -> r(MGI:Hnf1b)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.554+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Gata6) -> r(MGI:Hnf1b)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15542856

4
value: In contrast to Sox7, exogenous expression of Gata-4 or Gata-6 induced the expression of laminin alpha1 and Hnf1b in undifferentiated F9 and F9H1Sox7 cells without RA/Bt2cAMP treatment (Fig. 5 and 6 ).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15542856

Selventa

RAKAwdJbT6bEQCEUe2x3imTF9vdhDWwYhXfu8A08nA3PQ
has assertion: tscript(complex(NCM:"AP-1 Complex")) -> r(MGI:Pon2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.563+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCM:"AP-1 Complex")) -> r(MGI:Pon2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15544923

4
value: PON2 expression was found to be regulated, at least in part, by the transcription factor AP-1, as suggested by decreased JDP2 (AP-1 repressor) protein expression in the nucleus and by decreased PON2 expression in the presence of a Jun N-terminal kinase inhibitor (SP600125)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15544923

Selventa

RAEAD6cH4v9diE pxOxI8mRVO6ltjTHsVovwlYnlwcnZM
has assertion: bp(GO:"response to oxidative stress") -| cat(p(MGI:Ndufs2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.566+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to oxidative stress") -| cat(p(MGI:Ndufs2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15544925

4
value: we determined whether the oxidative stress that occurs in response to T. cruzi infection contributes to the catalytic impairment of respiratory complexes and to subsequent mitochondrial dysfunction in murine myocardium. Our data show that oxidative injuries, as determined by the levels of lipid peroxides and protein carbonyls, are incurred in cardiac mitochondria as early as 3 days postinfection and persist throughout the infection and disease. We observed substantial carbonylation of the specific subunits of mitochondrial respiratory complexes in infected murine hearts. Of note is the oxidative modification of NDUFS1, NDUFS2, and NDUFV1, which form the catalytic core of the CI complex; UQCRC1, UQCRC2, and UQCRQ, the subunits of the core subcomplex, and UQCRH and CYC1, which form the cyt c(1) subcomplex of CIII; and a gamma chain that is essential for ATP synthesis by CV complex. The extent of oxidative modifications of the subunits correlated with the catalytic defects of the respiratory complexes in the infected myocardium. Taken together, our data demonstrate that respiratory complexes are oxidatively damaged in response to the stress of T. cruzi infection. These data also suggest involvement of the specific susceptibility of the protein subunits, and not generalized mitochondrial oxidative damage in respiratory chain impairment of chagasic hearts.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15544925

Selventa

RAO E cnAupvpu7ll Ii6psY HQSp6mlb6QIxYP8erRTY
has assertion: cat(p(HGNC:PREX1)) => gtp(p(HGNC:RAC1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.569+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:PREX1)) => gtp(p(HGNC:RAC1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15545267

6
value: P-Rex1 is a guanine-nucleotide exchange factor (GEF) for the small GTPase Rac.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15545267

Selventa

RAKHtJ826aaMxba3Qfrx 1w2EqXfRFEasTLZ7ofpdEcwc
has assertion: kin(p(HGNC:ROCK1)) -| phos(p(HGNC:PPP1CB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.572+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ROCK1)) -| phos(p(HGNC:PPP1CB))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15545284

6
value: The gene silencing of p116Rip consistently and significantly increased myosin phosphorylation as well as stress fiber formation in cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15545284

Selventa

RAEVM5df6yA1-myDZ0tJ5yvQKCUAx2wO gX7VFRyDgeW8
has assertion: kin(p(HGNC:ROCK1)) -| phos(p(HGNC:PPP1CB))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.575+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ROCK1)) -| phos(p(HGNC:PPP1CB))
label: p(EGID:23164) -| (kin(p(HGNC:ROCK1)) -| phos(p(HGNC:PPP1CB)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15545284

8
value: The gene silencing of p116Rip consistently and significantly increased myosin phosphorylation as well as stress fiber formation in cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15545284

Selventa

RAJcxNe69HQMZTPH7K0Tmv727z-pk8Mtss7yQcnloRXcs
has assertion: tscript(complex(NCH:"Nfkb Complex")) => r(HGNC:XIAP)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.578+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCH:"Nfkb Complex")) => r(HGNC:XIAP)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15545623

4
value: Increased expression of the NF-kB target genes GADD45? (De Smaele et al. 2001; Papa et al. 2004) and XIAP (Tang et al. 2001) has been implicated in this process and it appears that NF-kB functions to suppress the TNF-stimulated ROS production that causes sustained JNK activation (Sakon et al. 2003).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15545623

Selventa

RAPRSdctBMpCVHT03Af8SZgWCN-ORzT-MSH17jZ3fEb2k
has assertion: p(MGI:Tnf) -> tscript(complex(NCM:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.586+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Tnf) -> tscript(complex(NCM:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15545623

4
value: Wild-type and Jnk1-/- Jnk2-/- (Jnk-/-) fibroblasts....Furthermore, TNF-stimulated NF-kB DNA binding activity was detected in nuclear extracts prepared from wild-type and Jnk-/- fibroblasts, but not from wild-type (N-IkBa) or Jnk-/- (N-IkBa) fibroblasts,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15545623

Selventa

RAG93a5JjyVg-y6UWIIRy-R7wlBqQj1GOY0V0nZF0HLak
has assertion: bp(MESHPP:"Liver Regeneration") -> r(MGI:Ctgf)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.592+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(MESHPP:"Liver Regeneration") -> r(MGI:Ctgf)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15546871

3
value: We performed microarray-based expression profiling on livers 0-40 h post-hepatectomy corresponding to G0, G1, and S phases. # supplemental data table
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15546871

Selventa

RAKTXOjP4y6GvrOqYD9UK71EkFnk6kdwxkS65KhgWkZlc
has assertion: bp(GO:"response to endoplasmic reticulum stress") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.602+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to endoplasmic reticulum stress") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15546873

2
value: Interestingly, ER stress stimulated SMC apoptosis, as demonstrated by annexin V binding, caspase-3 activation, and DNA laddering. The induction of apoptosis by ER stress was potentiated by HO inhibition, whereas it was prevented by addition of HO substrate.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15546873

Selventa

RAGv 7DOqv5fSSEO5e5s79KFqerABnYRcr Gg4k-Tv6wk
has assertion: cat(p(HGNC:ARAP3)) =| gtp(p(HGNC:RHOA))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.608+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:ARAP3)) =| gtp(p(HGNC:RHOA))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15546919

6
value: ARAP3 causes a Rho GAP-dependent decrease in active RhoA and Rac1 in vivo. ARAP3 stimulated a marked decrease in active RhoA levels in cells.ARAP3 showed GAP activity towards RhoA in vitro (our results) (Krugmann et al., 2002Go), and when overexpressed, inhibited actin stress fibre formation in PAE (Krugmann et al., 2002Go) and NIH3T3 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15546919

Selventa

RAHLLBgn krmxPh4iWFhFCD7YGljxMtuvGYsYpnbbCBxQ
has assertion: kin(p(HGNC:MAP2K6)) => kin(p(HGNC:PAK7))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.662+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAP2K6)) => kin(p(HGNC:PAK7))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15550393

6
value: PAK4 and PAK5 were similarly activated by MKK6, consistent with a conserved TPY motif in their activation domains.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15550393

Selventa

RAImHRG5hg17fueq8O7eWI7Wfq 5tg6dk2akEvNWUjN4g
has assertion: tscript(complex(NCH:"AP-1 Complex")) -> r(HGNC:CAPG)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.669+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(complex(NCH:"AP-1 Complex")) -> r(HGNC:CAPG)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15554385

4
value: \"Critical regulation of genes for tumor cell migration by AP-1.\" Strikingly, at low levels GFP-aFos, but not GFP-TAM67, caused a change in colony morphology, impairment of directional motility in a monolayer wound healing assay, as well as inhibition of chemotaxis and haptotaxis. Microarray analysis identified a novel set of AP-1 target genes, including the tumor suppressor TSCL-1 and regulators of actin cytoskeletal dynamics, including the gelsolin-like actin capping protein CapG.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15554385

Selventa

RAOLZWdUaNskXTFheP7VW5oySLt6a2yKfWa-dt7UTHVUQ
has assertion: p(EGID:313729) -| (p(RGD:Egf) -> kin(p(PFR:"Mapk JNK Family")))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.685+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:313729) -| (p(RGD:Egf) -> kin(p(PFR:"Mapk JNK Family")))
label: p(RGD:Egf) -> kin(p(PFR:"Mapk JNK Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15556944

7
value: Gene 33 inhibits EGFR autophosphorylation and specifically blunts epidermal growth factor (EGF)-induced activation and/or phosphorylation of Ras, ERK, JNK, Akt/PKB, and retinoblastoma protein.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15556944

Selventa

RAKdZFThVNU7oekT0pKxsCgsYn0cJXWZkUXCiQnzhnNHg
has assertion: p(EGID:313729) -| (p(RGD:Egf) -> kin(p(RGD:Mapk1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.687+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:313729) -| (p(RGD:Egf) -> kin(p(RGD:Mapk1)))
label: p(RGD:Egf) -> kin(p(RGD:Mapk1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15556944

7
value: Gene 33 inhibits EGFR autophosphorylation and specifically blunts epidermal growth factor (EGF)-induced activation and/or phosphorylation of Ras, ERK, JNK, Akt/PKB, and retinoblastoma protein.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15556944

Selventa

RAKnsi8ya5S6bLWMm00ssLJ83lL pdiVOcBErdS2XOHrU
has assertion: p(MGI:Csf3) -> p(MGI:Fli1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.702+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Csf3) -> p(MGI:Fli1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557108

4
value: Our results demonstrated that levels of Fli-1 protein, but not RNA, were higher in extracts from cells treated with G-CSF.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557108

Selventa

RAObOhyDgSloSAzjpsH31Au5771Nf1fp6gfQZspZ2EbJg
has assertion: path(MESHD:Ischemia) -> r(EGID:7916)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.713+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(EGID:7916)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: TABLE 3. Gene Expression Prediction Profile [changed in ischemic cardiomyopathy vs. non-ischemic] upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAHigopDp31ghe290tp2C8J6mmAS2hdpFC4mFdN9eznic
has assertion: path(MESHD:Ischemia) -> r(HGNC:CIZ1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.717+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(HGNC:CIZ1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: TABLE 3. Gene Expression Prediction Profile [changed in ischemic cardiomyopathy vs. non-ischemic] upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAEn-SVDrPGGP3dMUmafB8qp-S-oxiTDBSzQk8wPncH7M
has assertion: path(MESHD:Ischemia) -> r(HGNC:CNPY4)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.719+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(HGNC:CNPY4)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: TABLE 3. Gene Expression Prediction Profile [changed in ischemic cardiomyopathy vs. non-ischemic] upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAIqOKBGTYKUTZ6ee0HAony7VbmUhAoL5bV5gGIl7KjAk
has assertion: path(MESHD:Ischemia) -> r(HGNC:DOHH)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.720+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(HGNC:DOHH)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: TABLE 3. Gene Expression Prediction Profile [changed in ischemic cardiomyopathy vs. non-ischemic] upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAMZ8kmXRN642r5P0CFa3vztmdlKDRIMN zIQFJQRLEE8
has assertion: path(MESHD:Ischemia) -> r(HGNC:MAP2K7)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -> r(HGNC:MAP2K7)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: TABLE 3. Gene Expression Prediction Profile [changed in ischemic cardiomyopathy vs. non-ischemic] upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAGLasuQdeLCLAuNs4CkUs vhCK4XFtER2fr9eNk15eSg
has assertion: path(MESHD:Ischemia) -| r(HGNC:SACM1L)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.748+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(MESHD:Ischemia) -| r(HGNC:SACM1L)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557369

3
value: down
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557369

Selventa

RAIIB81Pv 4ujiKxoCAlX8AYSptCbvlV4FzfMWnFnNcIo
has assertion: a(CHEBI:lipopolysaccharide) -> r(MGI:Fcer2a)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.752+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(MGI:Fcer2a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557650

3
value: From full text Table 1. by Simon Dao
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557650

Selventa

RALKxrCkMBMCbmtlDe3tpOjFG2Io0GKSkbfpGIOLhtxak
has assertion: a(CHEBI:lipopolysaccharide) -> r(MGI:Nfkb2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.762+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(MGI:Nfkb2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557650

3
value: From full text Table 1. by Simon Dao
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557650

Selventa

RAP5RAvodzChuCWwXOALVkVcWNE1jfwoFbOkIGFfaMZTw
has assertion: a(CHEBI:lipopolysaccharide) -> r(MGI:Saa1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.763+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:lipopolysaccharide) -> r(MGI:Saa1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15557650

3
value: From full text Table 1. by Simon Dao
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15557650

Selventa

RAKCvJQvnemxTOCk0PWO1ex7cfM42eyAPDQIpv8fhWEQA
has assertion: p(HGNC:FGR) -> gtp(p(HGNC:RAC1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.809+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:FGR) -> gtp(p(HGNC:RAC1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15561106

5
value: Fgr increased Rac GTP loading, and phosphorylation of the Rac GEF Vav2, and bound to a protein complex formed by the Rho inhibitor p190RhoGAP and FAK, increasing p190RhoGAP phosphorylation, in a manner absolutely dependent on membrane localization.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15561106

Selventa

RAKyc6cAsfQtUzA9YHIajwfldYcqYDrBP5bJS6pI aPvo
has assertion: a(SCHEM:Epinephrine) -> path(SDIS:"adipocyte lipolysis")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.837+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Epinephrine) -> path(SDIS:"adipocyte lipolysis")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15564439

2
value: E2 can indirectly affect - by inducing the lipolytic enzyme hormone-sensitive lipase (31) or by increasing the lipolytic effects of epinephrine (32).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15564439

Selventa

RAP1Wo6dbuYLwUtN6ZJKCAespQopCXgn1fuoSl3xywHkI
has assertion: cat(p(HGNC:LPL)) -> path(SDIS:"fatty acid import")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.842+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:LPL)) -> path(SDIS:"fatty acid import")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15564439

4
value: This action happens principally through decreasing activity of lipoprotein lipase (LPL), an enzyme that regulates lipid uptake by adipocytes. Ovariectomy increases LPL and lipid deposition within the adipocyte and administering physiological doses of E2 reverses this deposition (29). Recently, work on a 3T3 adipocyte cell line transfected with estrogen receptor showed that the LPL gene has a negatively controlled estrogen response element (30).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15564439

Selventa

RAG6qWqpw8IZMSqGW5Me2Y0VgPEVFDd1UPY3S8DXvLT88
has assertion: complex(p(HGNC:CDKN2A),p(HGNC:BCL6)) -| tscript(p(HGNC:BCL6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.845+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:CDKN2A),p(HGNC:BCL6)) -| tscript(p(HGNC:BCL6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567177

7
value: Either mouse p19(ARF) or human p14(ARF) binds to BCL6 and downregulates BCL6-induced transcriptional repression.ARF-mediated downregulation of the BCL6 activity may account in part for ARF-mediated tumor suppression.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567177

Selventa

RAJIguySWE8kPheIEZ-qvaGrVl21vaD7YknUl7nyFMgxQ
has assertion: a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate") => kin(p(HGNC:AKT3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.850+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"Phosphatidylinositol-3,4,5-trisphosphate") => kin(p(HGNC:AKT3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

4
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAFbGidwvI02LWjsaQ4m02S92bQ2XSbobirFvxC4iNmVk
has assertion: cat(p(HGNC:SOS1)) => gtp(p(HGNC:KRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.858+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SOS1)) => gtp(p(HGNC:KRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

6
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAJ9-BCmI7BDy3zSdKiOFIGlO741aqWj9HnXuAAC2bXa8
has assertion: cat(p(HGNC:SOS1)) => gtp(p(HGNC:NRAS))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.859+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:SOS1)) => gtp(p(HGNC:NRAS))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

6
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAOnprc2cwawUeTdn8Zgfj15WuQ6dtCuFX28gDl3Ww8R0
has assertion: gtp(p(PFH:"RAS Family")) => kin(p(PFH:"RAF Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.862+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFH:"RAS Family")) => kin(p(PFH:"RAF Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

6
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAKtZmd5Vg7AR3XRBJiqMx4gaqkokLwpxwgEi BT1ldTM
has assertion: kin(p(HGNC:PDPK1)) => kin(p(HGNC:AKT1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.872+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PDPK1)) => kin(p(HGNC:AKT1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

6
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RANmCWWZqyD2CsRu6fFHgnIaNMyCPnI3oc3n44wrTtPn8
has assertion: kin(p(HGNC:PDPK1)) => kin(p(HGNC:AKT3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.875+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PDPK1)) => kin(p(HGNC:AKT3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15567848

6
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAIoK0rjysXep814LCSH1mnW48QgReEzuARa1lheumquc
has assertion: kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> kin(p(PFH:"AKT Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.876+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/15567848

5
value: Fig.1
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15567848

Selventa

RAMykFbyrXExWq137rtbqSDSCCED6WlyZ93FZ0LsCuB4Y
has assertion: a(SCHEM:Geldanamycin) -> (p(HGNC:EGF) -> kin(p(HGNC:MAPK1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.890+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Geldanamycin) -> (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/15568014

6
value: the activation of Erk and phospholipase C (PLC)-g observed following stimulation of HeLa cells with a low dose of EGF was accelerated and potentiated following co-treatment with a low dose of GA (Fig 2E).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15568014

Selventa

RAPEXioEDp2JnK-1yhk9Vd5shEggbf9LTsNya37zg3JrA
has assertion: kin(p(HGNC:MAPK3)) -> kin(p(HGNC:RPS6KA5))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.894+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:MAPK3)) -> kin(p(HGNC:RPS6KA5))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15568999

6
value: In the present study, we show that, in addition to being phosphorylated on Thr-581 and Ser-360 by ERK1/2 or p38,
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15568999

Selventa

RAOVQWwEKHtlTLT4fMlUmoA5 0 n XZ gB191brQ4DfQc
has assertion: p(HGNC:PXN,pmod(P,Y,31)) -> gtp(p(HGNC:RAC1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.930+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:PXN,pmod(P,Y,31)) -> gtp(p(HGNC:RAC1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15572663

5
value: We show that EGF stimulation activates the catalytic activity of Brk, which in turn phosphorylates paxillin at Y31 and Y118. These phosphorylation events promote the activation of small GTPase Rac1 via the function of CrkII
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15572663

Selventa

RAJES47w1NEtrq25U1oKGdAM6SqU--jgsTPJS9mFNTn9c
has assertion: tscript(p(MGI:Ep300)) -> tscript(p(PFM:"Tcf/Lef Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.933+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Ep300)) -> tscript(p(PFM:"Tcf/Lef Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15572674

6
value: It has been shown that the LIM protein FHL2 and the acetyltransferase CBP/p300 individually stimulate beta-catenin transactivating activity
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15572674

Selventa

RAFVf4bRqu9QdH11xJE2 5lgsxLYVjY3d -Q0efP-nRZM
has assertion: kin(p(MGI:Raf1)) -> kin(p(PFM:"MEK1/2 Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.937+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Raf1)) -> kin(p(PFM:"MEK1/2 Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15572689

6
value: Although activation of RAF and AKT is clearly sufficient to repress p27Kip1 expression, these experiments do not address whether the PI3'-kinase-PDK1-AKT and the RAF-MEK- ERK pathways are required for the repression of p27Kip1 in response to mitogenic stimulation or oncogenic transformation. To address this, we used pharmacological inhibitors of the signaling proteins PI3'-kinase (LY294002), mTor (rapamycin), and MEK (PD98059, U0126, or CI-1040) either alone or in combination with one another. PDGF stimulation of quiescent NIH 3T3 cells leads to activation of both the PI3'-kinase- PDK1-AKT and the RAF-MEK-ERK signaling pathways and repression of p27Kip1 expression (Fig. 3A).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15572689

Selventa

RAIrvsVFMnrcQ6SquOZHsn3nGsMNTtSVuY9GBdMNo4Ohc
has assertion: kin(p(MGI:Raf1)) -| bp(GO:"G1/S transition of mitotic cell cycle")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.944+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Raf1)) -| bp(GO:"G1/S transition of mitotic cell cycle")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15572689

4
value: Moreover, AKT was able to bypass RAF-induced G1 cell cycle arrest mediated by CKI-dependent inhibition of cyclin E/cdk2 (64).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15572689

Selventa

RAHOTgX68cvZxEK-R958GzFMTQBOsax0oJ5KUK8zc114w
has assertion: gtp(p(MGI:Rhoa)) -| (gtp(p(PFM:"Ras Family")) -> r(MGI:Cdkn1a))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.947+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(MGI:Rhoa)) -| (gtp(p(PFM:"Ras Family")) -> r(MGI:Cdkn1a))
label: gtp(p(PFM:"Ras Family")) -> r(MGI:Cdkn1a)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15572689

8
value: Under these circumstances activated RhoA is reported to prevent the expression of the CKI p21Cip1, a major mediator of RAS- or RAF-induced cell cycle arrest in mouse fibroblasts (43).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15572689

Selventa

RAFgKcPhTzLNGxGR-aawbp2SUkEBUrMHotI0wj-9KtCb4
has assertion: kin(p(HGNC:ROCK1)) => kin(p(HGNC:LIMK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.953+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ROCK1)) => kin(p(HGNC:LIMK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15573116

6
value: ROCK1 and -2, alternatively, activate LIM domain-containing protein kinase 1 (LIMK1) and 2 (LIMK2), which phosphorylate and inhibit the actin depolymerization factor cofilin (cofilin-P). This increases actin polymerization and results in the stabilization of actin stress fibres27. The phosphatase slingshot dephosphorylates cofilin, which blocks actin polymerization.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15573116

Selventa

RANdBNn3LHiN7L10fyoovrZxnokkf74DQbYLnFywlHr8k
has assertion: p(HGNC:CDKN1A) =| kin(p(HGNC:ROCK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.954+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CDKN1A) =| kin(p(HGNC:ROCK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15573116

5
value: Whereas the function of CKIs as tumour suppressors is well characterized in the nucleus, they also seem to function in the cytoplasm,where they regulate cytoskeletal functions. This occurs through the modulation of the Rho signalling pathway. This cytoplasmic function could be oncogenic, as inhibition of the Rho pathway can result in increased migratory capacity. Phosphorylation of p21 on Thr145 by protein kinase B (PKB)/Akt48 or Pim1 inhibits the nuclear localization of p21. In the cytoplasm, p21 can protect the cell from apoptosis, as well as bind and inhibit the Rho kinases ROCK1 and -2 to modulate actin cytoskeleton organization46,47.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15573116

Selventa

RAOK0inq7pDADdqkAW5LQBa 44IVjV5K8EwTTZHBvZM78
has assertion: tloc(p(HGNC:CDKN1A),GOCCACC:"GO:0005634",GOCCACC:"GO:0005737") -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.957+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(HGNC:CDKN1A),GOCCACC:"GO:0005634",GOCCACC:"GO:0005737") -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15573116

4
value: Whereas the function of CKIs as tumour suppressors is well characterized in the nucleus, they also seem to function in the cytoplasm,where they regulate cytoskeletal functions. This occurs through the modulation of the Rho signalling pathway. This cytoplasmic function could be oncogenic, as inhibition of the Rho pathway can result in increased migratory capacity. Phosphorylation of p21 on Thr145 by protein kinase B (PKB)/Akt48 or Pim1 inhibits the nuclear localization of p21. In the cytoplasm, p21 can protect the cell from apoptosis, as well as bind and inhibit the Rho kinases ROCK1 and -2 to modulate actin cytoskeleton organization46,47.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15573116

Selventa

RALuClo7lHgYGyA410ckxhfwKfvycRDdaFwS-FD751GyY
has assertion: bp(GO:aging) -> r(HGNC:ATRX)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.972+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:ATRX)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAGy2LlDwfz-NSWLPLq7lBbL6aRhJdcfKsir1ngz7nUG8
has assertion: bp(GO:aging) -> r(HGNC:H2AFY2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.973+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:H2AFY2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RANEKVb6xuh0pyQZ08Gc7ZlWmQwvHmP6RQNxxF3uusZK4
has assertion: bp(GO:aging) -> r(HGNC:H3F3A)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.974+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:H3F3A)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAOIn9IgAdh985NArYgG0INkNnp0wxqUQRa-bHclN Wrk
has assertion: bp(GO:aging) -> r(HGNC:NBL1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.977+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:NBL1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAGNF57lnk2KXRrnhZRfrtvc60A-bsL180JV9KdAlAxqo
has assertion: bp(GO:aging) -> r(HGNC:RBM5)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.980+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -> r(HGNC:RBM5)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAGXaYDcDsvwompsvgPzYfg8RaGtED3e2QMoylrzenyGk
has assertion: bp(GO:aging) -| r(HGNC:BCL2A1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.986+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:BCL2A1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAH jVvx3vGweyyfdtVGDlDvCmCgA-iQCvNVVTS5o4Jjk
has assertion: bp(GO:aging) -| r(HGNC:CCNB1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.988+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:CCNB1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAHFxVS-iJDl4BVknnDSvIEemIQApDZY0dUgM6Kx3PoUw
has assertion: bp(GO:aging) -| r(HGNC:DNMT3B)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.990+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:DNMT3B)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAL5U8XDOWeaFOP7PbC2kmYI-C2ER2lQsEDQq5-lX6Ohg
has assertion: bp(GO:aging) -| r(HGNC:PER2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.997+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:PER2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAPnApKygWIEkYk7FAaggb4TtQPxgkClSld jAmesyRPA
has assertion: bp(GO:aging) -| r(HGNC:TRAP1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:29.999+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:aging) -| r(HGNC:TRAP1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574761

3
value: downregulated
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574761

Selventa

RAH9Q5pZqbisaNf9bgv5wvRTCQWXJ29QI1TJKlQAVF-IE
has assertion: kin(p(HGNC:PRKCD)) -> tloc(p(HGNC:FGF1),GOCCACC:"GO:0005634",GOCCACC:"GO:0005737")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.003+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKCD)) -> tloc(p(HGNC:FGF1),GOCCACC:"GO:0005634",GOCCACC:"GO:0005737")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15574884

6
value: Fibroblast growth factor-1 (FGF-1), which stimulates cell growth, differentiation, and migration, is capable of crossing cellular membranes to reach the cytosol and the nucleus in cells containing specific FGF receptors. The cell entry process can be monitored by phosphorylation of the translocated FGF-1. We present evidence that phosphorylation of FGF-1 occurs in the nucleus by protein kinase C (PKC)delta. The phosphorylated FGF-1 is subsequently exported to the cytosol
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15574884

Selventa

RAMrSIbsY6y4lbOjM4xVn80-pRhcROvHlPBTDDFd8pQ5s
has assertion: p(HGNC:STXBP3,pmod(P)) -> bp(GO:"cell adhesion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.016+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:STXBP3,pmod(P)) -> bp(GO:"cell adhesion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15576373

3
value: Thus, protease-activated receptor-1-induced protein kinase Calpha activation and phosphorylation of syntaxin 4 and Munc18c are required for the cell surface expression of P-selectin and the consequent binding of neutrophils to endothelial cells.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15576373

Selventa

RAOzhQCcER1ka04HDKhktqBnp1T8U4Mj6tKlKpXm5po8g
has assertion: bp(GO:"muscle contraction") -| r(RGD:Mmp2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.036+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"muscle contraction") -| r(RGD:Mmp2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15578428

3
value: In a rat tail-suspension experimental model, we show that after fourteen days of non-weight bearing there is increased expression of MMP-2 in the atrophic soleus and gastrocnemius and decreased expression of TIMP-2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15578428

Selventa

RAEoBd35oS1BC2-eeF7CcQGLF5 0giS-9y-DujbM10qK8
has assertion: p(HGNC:TOM1L1) -> kin(p(HGNC:SRC))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.045+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TOM1L1) -> kin(p(HGNC:SRC))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15579470

5
value: Data presented here demonstrate that epidermal growth factor (EGF) receptor ligands promote the tyrosine phosphorylation of endogenous and adenovirally transduced Srcasm in keratinocytes, and that increased levels of Srcasm activate endogenous SFKs, with a preference for Fyn and Src.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15579470

Selventa

RAFm1GadKYoWcNlzlCK9GrUiO42whevCX60VxAdLItzUQ
has assertion: a(CHEBI:"vitamin E") -| (p(EGID:2357) -> a(CHEBI:"leukotriene B4"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.052+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"vitamin E") -| (p(EGID:2357) -> a(CHEBI:"leukotriene B4"))
label: p(EGID:2357) -> a(CHEBI:"leukotriene B4")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15579728

4
value: Furthermore, whereas LTB4 production by neutrophils from control subjects was concentration dependently inhibited by the lipophilic antioxidant -tocopherol (Figure 3),
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15579728

Selventa

RAEpVivvTsqi2UtbIWKyxfCOezzpKd7rYl6AKziU8xcnU
has assertion: kin(p(HGNC:ERBB2)) -> bp(GO:"cell-cell adhesion")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.060+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ERBB2)) -> bp(GO:"cell-cell adhesion")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15579904

4
value: erbB2, the ligand-less member of the epidermal growth factor receptor family, was shown to form a complex with the hemidesmosomal integrin alpha6beta4. These results indicate that stimulation of alpha6beta4 increases E-cadherin-mediated cell-cell adhesion and that this mechanism depends on erbB2 activation.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15579904

Selventa

RAI5dxPa1Fo-IoI09MCvkhdsrS4IxEBmK 4Mad1zO76wY
has assertion: p(HGNC:NLRC4) -> (p(HGNC:TP53) -> bp(MESHPP:Apoptosis))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.066+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NLRC4) -> (p(HGNC:TP53) -> bp(MESHPP:Apoptosis))
label: p(HGNC:TP53) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15580302

5
value: A dominant-negative mutant of Ipaf inhibited p53-induced and doxorubicin-induced apoptosis by about 50%.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15580302

Selventa

RANm1rSfZpfyYmSRpcEGYXWuDsIJmWMiEHhGCZp8Rtcko
has assertion: p(HGNC:UNC13D) -> bp(GO:phagocytosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.076+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:UNC13D) -> bp(GO:phagocytosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15582491

3
value: The accurate killing is assured by a vectorial movement of secretory lysosomes along microtubules and focused secretion within the immunological synapse. Here we present an over view of how these key regulators such as AP-3 adaptor protein, RabGGTase enzyme, Rab27a small GTP binding protein, Lyst and Munc13-4 act in a very orchestrated way to deliver the kiss of the death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15582491

Selventa

RAG5uUo5JzUSQahIYDcCSt797MY7nnEZ4xrBTrjJ0t68Y
has assertion: p(HGNC:NF1) -| kin(p(PFH:"MAPK JNK Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.082+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:NF1) -| kin(p(PFH:"MAPK JNK Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583854

5
value: Alternatively, Kit signaling may also activate JNK kinase, a MAP kinase activated in response to stress [35]. NF1, a GTPase activating protein, is considered to be involved in modulating Ras activation through Kit signaling [36]. NF1 deficiency that occurs in cases of neurofibromatosis may induce an increase in MAP kinase activity. Pathways with JAK/STAT or with Src family members may be involved in Kit signaling [33] (fig. 1). Some studies showed the association of JAK2 with Kit and also its activation by Kit signaling [37]. Other reports also indicated the increased activity of Lyn, a Src family member, by Kit signaling [38].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583854

Selventa

RAKx 32Xb68N1OiLp3YLSziM0POcLUW3Q2oz78EzNzQKg
has assertion: p(PFH:"AKT Family",pmod(P,Y)) -| bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.092+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFH:"AKT Family",pmod(P,Y)) -| bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583854

3
value: Binding of dimerized KitL induces the dimerization of Kit [32]. This leads to the autophosphorylation of Kit on tyrosine and its association with substrates of various kinds. The phophatidylinositol-3-kinase (PI3K)/Akt system is one of the major pathways [33] (fig. 1). PI3K is composed of an 85-kDa regulatory subunit and a 110-kDa catalytic subunit. The 85-kDa regulatory subunit is associated with activated Kit through an SH2 domain, and then is phosphorylated on tyrosine. The 110-kDa catalytic subunit of the activated PI3K produces phosphatidylinositol-3,4-bisphosphate, which in turn is used for phosphorylation of Akt, a serine-threonine kinase. The activated Akt is involved in the inhibition of apoptosis of cells whose survival depends on Kit signaling. A tyrosine kinase inhibitor, imatinib mesylate blocks not only autophosphorylation of Kit but also phosphorylation of Akt [34]. Induction of apoptosis in Kit signaling-dependent cells by imatinib mesylate may be mediated through the inhibition of Akt activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583854

Selventa

RANgEjT0rEONIiwBnMOqorzuc3cKey7HrpRkJW2uG8654
has assertion: p(HGNC:KIT,pmod(P,Y)) => kin(p(HGNC:KIT))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.095+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:KIT,pmod(P,Y)) => kin(p(HGNC:KIT))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583854

5
value: Binding of dimerized KitL induces the dimerization of Kit [32]. This leads to the autophosphorylation of Kit on tyrosine and its association with substrates of various kinds. The phophatidylinositol-3-kinase (PI3K)/Akt system is one of the major pathways [33] (fig. 1). PI3K is composed of an 85-kDa regulatory subunit and a 110-kDa catalytic subunit. The 85-kDa regulatory subunit is associated with activated Kit through an SH2 domain, and then is phosphorylated on tyrosine. The 110-kDa catalytic subunit of the activated PI3K produces phosphatidylinositol-3,4-bisphosphate, which in turn is used for phosphorylation of Akt, a serine-threonine kinase. The activated Akt is involved in the inhibition of apoptosis of cells whose survival depends on Kit signaling. A tyrosine kinase inhibitor, imatinib mesylate blocks not only autophosphorylation of Kit but also phosphorylation of Akt [34]. Induction of apoptosis in Kit signaling-dependent cells by imatinib mesylate may be mediated through the inhibition of Akt activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583854

Selventa

RAK8OiyAAzRDUasBqYtDGCatZ8zjezR-l5wSnhI5GelOk
has assertion: p(HGNC:KIT,pmod(P,Y)) => kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.096+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:KIT,pmod(P,Y)) => kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583854

4
value: In human mast cell leukemia cell line, HMC-1, Kit was const phosphorylated on tyrosine, activated and then could associate with PI3K without addition of KitL.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583854

Selventa

RAFrIw dYSJng2mpNn0UoiwmzO7M gTtsV2AU3H15lAhA
has assertion: cat(p(HGNC:EDNRB)) -> kin(p(HGNC:RET))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.101+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:EDNRB)) -> kin(p(HGNC:RET))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583857

6
value: EDNRB activation enhances the effects of RET signaling on the proliferation of uncommitted ENS neurons but inhibits RET-mediated chemoattractive effects [19].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583857

Selventa

RALyZR61Jgh1pC4RFASpwyKtRHgM6ae7qewYRFZn9FP g
has assertion: cat(p(HGNC:EDNRB)) -| a(SCHEM:"cyclic AMP")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.103+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:EDNRB)) -| a(SCHEM:"cyclic AMP")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583857

4
value: EDNRB reduces cyclic AMP (cAMP) production via Gai, thus leading to protein kinase A (PKA) inhibition. Since chemical PKA blockade mimics the effects exerted by ET-3 on ENS progenitors, it is likely that the RET-EDNRB interaction is mediated by PKA (fig. 1) [19]. This is supported by the finding that serine 686 in the juxtamembrane domain of RET is phosphorylated by PKA, thereby enhancing RET-mediated lamellipodia formation [20].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583857

Selventa

RAJxeSWPan-hN-7beJEhxbb2Tx5HlZ9xLHVTLaC9YXX94
has assertion: cat(p(HGNC:GFRA1)) -> kin(p(HGNC:SRC))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.107+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:GFRA1)) -> kin(p(HGNC:SRC))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583857

6
value: GDNF signaling needs heparan sulphate glycosaminoglycans, such as syndecans and glypicans, probably to ensure local concentration of GDNF [26]. GDNF is able to trigger intracellular signaling events that are mediated by GFR-a but not by RET [27]. Stimulated GFR-a can trigger c-Src activation; in turn, c-Src induces phosphorylation of Met, the tyrosine kinase receptor of hepatocyte growth factor (HGF) [28]. Thus, Met may contribute to RET-independent GDNF signaling (fig. 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583857

Selventa

RAFgqzMYcAHEaswfHkNrzqkt4bcRT0G5R5fw FmDh5Q7Q
has assertion: gtp(p(PFH:"RAS Family")) -> tscript(complex(NCH:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.111+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFH:"RAS Family")) -> tscript(complex(NCH:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15583857

5
value: RET stimulation triggers many other signaling intermediates, including CREB [42], p38MAPK [42], NFkB [43], ERK5 (BMK1) [44], phosphoinositide-dependent kinase 1 (PDK1) 45, cyclin-dependent kinase 5 (CDK5) [46] and PKC isoforms [47 48] (fig. 3). Although the mechanism of activation of these pathways remains to be elucidated, Y1062 is important for most of them. In particular, Ras/ERK- and PI3K-triggering by Y1062 is essential for full activation of CREB and NFkB [42]. A novel RET interactor designated Grap-2 has been found to negatively regulate NFkB activation [43].
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15583857

Selventa

RAMcItFlMenu3UloTDGOVpHTn4SLO0Oxpg0ASecMsMTpY
has assertion: p(HGNC:SPRY4) -| gtp(p(PFH:"RAS Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.130+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SPRY4) -| gtp(p(PFH:"RAS Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15584898

5
value: We previously showed that TESK1 interacts with Sprouty-4 (referred to as Spry4), an inhibitor of growth factor-induced Ras/MAP (mitogen-activated protein) kinase signalling, but the functional role of this interaction has remained unknown.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15584898

Selventa

RAIpbpye mQP5ybaiXf Ox-19ZQH1bz3KZ4BEfwIBV7M
has assertion: bp(GO:"response to endoplasmic reticulum stress") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.131+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to endoplasmic reticulum stress") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15585578

2
value: We and others have shown that ER stress can induce intracellular lipid accumulation through the activation of the sterol responsive element binding proteins (SREBPs) and initiate programmed cell death by activation of caspases
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15585578

Selventa

RAOj3i9O5n9RKZcrEO59jq4WCwnFzS1FYngp8KSMSBCbs
has assertion: p(MGI:Serpinb8) -> r(MGI:Cxcl12)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.162+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Serpinb8) -> r(MGI:Cxcl12)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15585884

4
value: while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15585884

Selventa

RAOZxCHoDiyyNceq1bMm-3izuuthMKz8WYakOh rBK7A
has assertion: p(MGI:Serpinb8) -> r(MGI:Cxcl13)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.164+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Serpinb8) -> r(MGI:Cxcl13)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15585884

4
value: while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15585884

Selventa

RAH8n ktGTo3gFTC2kJs3P7u72J rvd0jOS0B9Z1IbSkQ
has assertion: cat(p(HGNC:REN)) -> kin(p(HGNC:MAPK1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.169+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:REN)) -> kin(p(HGNC:MAPK1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15587681

6
value: Binding of (pro)renin to the receptor mediates (pro)renin cellular effects by activating MAP kinases ERK1/2.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15587681

Selventa

RAJLvOnAZNmzYJd3Tft1WotPqQhmdX5ujKrGxaWesYWrI
has assertion: p(HGNC:SREBF2,pmod(P,S,432)) => tscript(p(HGNC:SREBF2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.178+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:SREBF2,pmod(P,S,432)) => tscript(p(HGNC:SREBF2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15589694

5
value: insulin also stimulates the transcriptional activity of nSREB2 and nSREB1A through a mitogen activated protein kinase pathway. The ser117 residue has been identified as the major phosphorylation site for MAPK in SREB1A. Ser432 and Ser455 are described as the MAPK phosphorylation sites in viro and in vivo in SREBP2. These phosphorylations do not modify DNA binding but enhance SREBP2 transactivation capacity. A role for MAPK in the modification of SREB1C transcriptional activity remains controversial. Although the ser117 target of MAPK in SREBP1A is also present in the SREBP1C isoform, the use of inhibitors of teh MAPK pathway in cultured hepatocytes do not antagonize the effect of insulin on SREBP1C target genes, suggesting that SREBP1C is not phosphorylated by MAPK in hepatocytes. We have shown that PKB is able to phosphorylate purified nSREBP1C in vitro. Cotransfection experiments in cultured hepatocytes indicate that phosphorylation by insulin and PKB stimulates the transcriptional activity of nuclear SREBP1C
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15589694

Selventa

RANkSw4Cj5F1BA1PcLSfS2il6APJ9qHOIVCtfgciugfYE
has assertion: kin(complex(NCM:"p85/p110 PI3Kinase Complex")) -| r(MGI:Saa3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.190+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCM:"p85/p110 PI3Kinase Complex")) -| r(MGI:Saa3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15590982

4
value: Modified assertion
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15590982

Selventa

RAP2sQUbZRxYo687dOHckI iy94DQwzz8ipL2X95K-HxU
has assertion: complex(p(HGNC:FKBP5),p(PFH:"HSP90 Family")) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.192+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:FKBP5),p(PFH:"HSP90 Family")) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15591061

7
value: The Inhibitory Activity of FKBP51 Requires Interaction with Hsp90
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15591061

Selventa

RAFWEpmnCSSZsSD ghvY0nJGWUmbefhUSdKdJ9nMBzXWY
has assertion: p(HGNC:DCTN2) -| tscript(p(HGNC:NR3C1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.193+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:DCTN2) -| tscript(p(HGNC:NR3C1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15591061

5
value: dynamitin, which disrupts the transport complex and reduces receptor activity;
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15591061

Selventa

RAGq3ZoIfjOglPmXrQ P3dhX-9kcnMj6HDbvCBM-X3GE4
has assertion: kin(p(HGNC:ABL1)) => p(EGID:5424,pmod(P,Y,15))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.204+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:ABL1)) => p(EGID:5424,pmod(P,Y,15))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15591787

5
value: We show that Abi promotes Abl-mediated phosphorylation of Cdc2 at tyrosine 15 and inactivation of Cdc2 kinase activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15591787

Selventa

RAPXkfbNKCiApH9e7O6ohoOjyiGLcZFuIjM8cojLoe2Ps
has assertion: kin(p(MGI:Src)) -> p(MGI:Crkl,pmod(P,Y,251))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.207+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Crkl,pmod(P,Y,251))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: Supplementary Table 5
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAEOK5o6TSEnA0fZVYV4QnSN1EZy54Q-T4m7-r9h0IcAY
has assertion: kin(p(MGI:Src)) -> p(MGI:Anxa2,pmod(P,Y,238))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.215+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Anxa2,pmod(P,Y,238))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAMwH-fJQSivxIG9SVwUq8j3YUxpB BlmFHy-fyx5V6co
has assertion: kin(p(MGI:Src)) -> p(MGI:Cdc42bpb,pmod(P,Y,954))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.231+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Cdc42bpb,pmod(P,Y,954))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAE4ylyMf5SXMfTSPc6EOP49sImDjg3vFNo9A313DRP6Y
has assertion: kin(p(MGI:Src)) -> p(MGI:Ctnnd1,pmod(P,Y,221))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.233+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Ctnnd1,pmod(P,Y,221))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAM T 1riyP4XzmWLEfFRB83DzvOT3c17org17NTbsfkQ
has assertion: kin(p(MGI:Src)) -> p(MGI:D8Ertd82e,pmod(P,Y,437))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.238+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:D8Ertd82e,pmod(P,Y,437))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAJTEdIbYbIE-c1wdMLIO0IgD-h6J7MSZGNun77OFsrVw
has assertion: kin(p(MGI:Src)) -> p(MGI:Dok1,pmod(P,Y,361))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.284+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Dok1,pmod(P,Y,361))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RANH4 0RqHNKuptpvhNqslG0X7IDjgzDFSq jLUeG7LZU
has assertion: kin(p(MGI:Src)) -> p(MGI:Dok1,pmod(P,Y,408))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.289+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Dok1,pmod(P,Y,408))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAPCG3DSKDTINFCmKXNpQ5xOTvbTYNMYM2DPkIiIaRj8Q
has assertion: kin(p(MGI:Src)) -> p(MGI:Eps8,pmod(P,Y,490))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.299+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Eps8,pmod(P,Y,490))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAN89H0-NIvuXIZ3wMAOotXOmjpDYtsLDqe7bNTR4A-ps
has assertion: kin(p(MGI:Src)) -> p(MGI:Mgrn1,pmod(P,Y,394))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.317+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Mgrn1,pmod(P,Y,394))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAM4YP8nIzidHO7MftmOgX-PNXgvKzhYsz2qPH3eWTi 4
has assertion: kin(p(MGI:Src)) -> p(MGI:Pcdh1,pmod(P,Y,79))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.320+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Pcdh1,pmod(P,Y,79))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAJ7PFYs4dTUiw4Rua2xlKSjL7vpyw44UT zBpQeAplho
has assertion: kin(p(MGI:Src)) -> p(MGI:Phldb2,pmod(P,Y,130))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.325+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Phldb2,pmod(P,Y,130))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAP-2OlTbf6jyj1HEb3iKjiLQ4Y2hjKfXLv6FAVhJsIWM
has assertion: kin(p(MGI:Src)) -> p(MGI:Ptpn11,pmod(P,Y,62))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.335+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Ptpn11,pmod(P,Y,62))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAGAPBdlyyzbhxJFTRQ1QkCh5YJEJLybRgJQrxw1WTLUE
has assertion: kin(p(MGI:Src)) -> p(MGI:Rab7,pmod(P,Y,183))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.338+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Rab7,pmod(P,Y,183))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAOuYS78WAw4KuLzCLLFlD9qcE5B8ZNqNVL7r ohuBfSs
has assertion: kin(p(MGI:Src)) -> p(MGI:Scarf2,pmod(P,Y,615))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.342+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Scarf2,pmod(P,Y,615))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAO335BClvpmAdy7QtCJmbHb9jO0jWhqvkTZj RkonhYM
has assertion: kin(p(MGI:Src)) -> p(MGI:Skap2,pmod(P,Y,260))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.346+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Skap2,pmod(P,Y,260))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RALrJHlMZXUAeiParrPG57OVy7pxrr2fN7TYfRfj57DY0
has assertion: kin(p(MGI:Src)) -> p(MGI:Tjp1,pmod(P,Y,1164))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.353+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Tjp1,pmod(P,Y,1164))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAJYaMSGwAA8PFfLWSqeDogA0zzmaRIz-GUGWb4shknaw
has assertion: kin(p(MGI:Src)) -> p(MGI:Tjp1,pmod(P,Y,1177))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.355+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Tjp1,pmod(P,Y,1177))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RANyzOj3bPr5f9XJXQI7z uuHv6JJ6uA0Kq020pk CPxc
has assertion: kin(p(MGI:Src)) -> p(MGI:Tkt,pmod(P,Y,275))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.356+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Tkt,pmod(P,Y,275))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAKlR2bxZ6FMhp-9eItoycOE5la9VAon9 ZVHZmUX c-U
has assertion: kin(p(MGI:Src)) -> p(MGI:Twf2,pmod(P,Y,309))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.360+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(MGI:Src)) -> p(MGI:Twf2,pmod(P,Y,309))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592455

5
value: To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592455

Selventa

RAIkEAfc1Pvrb4KfL9UmSw0YiDiCIwWVCtxPC-tfsZu0E
has assertion: kin(p(HGNC:PRKDC)) -| cat(p(HGNC:PARP1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.370+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKDC)) -| cat(p(HGNC:PARP1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592499

6
value: Table 1 Substrates of DNA-PK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592499

Selventa

RAPjPVRjefIbCCpVanA8HJa0kgeuD2WkOq7O3qor-0DJM
has assertion: kin(p(HGNC:PRKDC)) -> tscript(p(HGNC:SRF))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.372+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PRKDC)) -> tscript(p(HGNC:SRF))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15592499

6
value: Table 1 Substrates of DNA-PK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15592499

Selventa

RAFyQCTyUOmXXhH1Whf7MtklhbQK1bFLoebz8GPEd4Eqc
has assertion: tscript(p(HGNC:ESRRA)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.381+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ESRRA)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598686

4
value: Transfection results showed that overexpression of ERRs inhibited cell proliferation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598686

Selventa

RAIAAbCoC2crKkli3 9NdtNNQ2j0uvaSNsNySpKTOnAEc
has assertion: tscript(p(HGNC:ESRRG)) -| bp(GO:"cell proliferation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.382+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:ESRRG)) -| bp(GO:"cell proliferation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598686

4
value: Transfection results showed that overexpression of ERRs inhibited cell proliferation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598686

Selventa

RALKWZWHua4c1GN5k1jR9OQwW0bQAdwyKVjs3crBus9rg
has assertion: kin(p(HGNC:PTK2)) => p(HGNC:PTK2,pmod(P,Y,397))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.386+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(HGNC:PTK2)) => p(HGNC:PTK2,pmod(P,Y,397))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598735

5
value: CrkII overexpression enhanced the autophosphorylation of FAK at Tyr-397 and tyrosine phosphorylation of p130(Cas) (Crk-associated substrate, Cas) upon stimulation of integrin by fibronectin.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598735

Selventa

RAHYVJCX8cxNLQ69Op6xsJ0JbPtMo-U1sBH4Ix Kcu1P8
has assertion: tscript(p(HGNC:SPI1)) -| p(HGNC:MAFB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.391+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:SPI1)) -| p(HGNC:MAFB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598817

5
value: DCs inducing levels of PU.1 inhibited MafB expression in monocytes, which appeared to be required for DC specification, since constitutive MafB expression inhibited DC differentiation. Consistent with this, PU.1 directly bound to MafB, inhibited its transcriptional activity in macrophages, and repressed its ability to induce macrophage differentiation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598817

Selventa

RAP7vijzGSPL33QFkipCAJr2JkmIZt3L07bGb3SEbIiDc
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:PTGS2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.395+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:PTGS2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Activation of the inducible form of cyclooxygenase, COX-2, and of the interleukins IL-1, IL-6, and IL-8, as well as of the NF-kappaB pathway, was observed preferentially in cells in contact with bacterial supernatant.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAFt7WPoO7KhH6vBBKcpkZ4ta7 5wp4ar69icV30v8R18
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:JUN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.398+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:JUN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Among others, Fos, Jun, and EGR-1 were upregulated by the bacterial supernatant and by live bacteria
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAPKWDENKMn3IYU6IaCu1g5aOvLq6yjbCCDaWPbaAmq-A
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:JUNB)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.402+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:JUNB)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Early infection was characterized by an upregulation of anti-apoptotic genes and a downregulation of pro-apoptotic genes. This correlated with a necrotic, rather than apoptotic cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RALkMAq6kzot cSDdLmeXGCmkluy0KFYHmJTmcmtQLuLQ
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:KLF6)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.403+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:KLF6)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Early infection was characterized by an upregulation of anti-apoptotic genes and a downregulation of pro-apoptotic genes. This correlated with a necrotic, rather than apoptotic cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAOExPWbYCIfGTf91UIU04p8GaU6ypV0beS6tCFOopNdo
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:MYC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.405+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:MYC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Early infection was characterized by an upregulation of anti-apoptotic genes and a downregulation of pro-apoptotic genes. This correlated with a necrotic, rather than apoptotic cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAEs6hLZFxPb aRKuyKRD-7pmll-v2POIpjZoXHqOK9d0
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:PIM1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.409+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:PIM1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Early infection was characterized by an upregulation of anti-apoptotic genes and a downregulation of pro-apoptotic genes. This correlated with a necrotic, rather than apoptotic cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAH OGAYfKPL-egiBnFOiRqOLOxrJPZL1MSYkiGNxhILc
has assertion: path(SDIS:"bacterial infection") -> r(HGNC:YARS)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.414+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:"bacterial infection") -> r(HGNC:YARS)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598879

3
value: Early infection was characterized by an upregulation of anti-apoptotic genes and a downregulation of pro-apoptotic genes. This correlated with a necrotic, rather than apoptotic cell death.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598879

Selventa

RAG7XOTFizpjVd3LH0L70dmqIcGm122MLm5Dwk54rrEhM
has assertion: bp(GO:"response to endoplasmic reticulum stress") -> tscript(p(MGI:Atf6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.419+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to endoplasmic reticulum stress") -> tscript(p(MGI:Atf6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598891

4
value: % ATF6 and XBP1 are transcription factors activated specifically in response to endoplasmic reticulum (ER) stress.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598891

Selventa

RAJBUSLwZ4d 0EutB 1gJwBnAEjZkwt6S4W15kMQGZw-0
has assertion: bp(GO:"response to endoplasmic reticulum stress") -> tscript(p(MGI:Xbp1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.420+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to endoplasmic reticulum stress") -> tscript(p(MGI:Xbp1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15598891

4
value: % ATF6 and XBP1 are transcription factors activated specifically in response to endoplasmic reticulum (ER) stress.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15598891

Selventa

RALo5tTDhwYRw LUj5gY6ghNh8pC9YEeW 5HUklEXtpwc
has assertion: a(CHEBI:"reactive oxygen species") -> r(MGI:Ccl2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.428+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"reactive oxygen species") -> r(MGI:Ccl2)
label: cat(complex(NCM:"NADPH Oxidase Complex")) -> (a(CHEBI:"reactive oxygen species") -> r(MGI:Ccl2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15599400

5
value: Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15599400

Selventa

RAL0uxgpYh32VTTEkjT7CjOMwo5GyfPFrE FZ2m2sVc5g
has assertion: a(CHEBI:"reactive oxygen species") -| r(MGI:Adipoq)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.433+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"reactive oxygen species") -| r(MGI:Adipoq)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15599400

3
value: The mRNA expression levels of adiponectin and PPARg were diminished by incubation with H2O2 (Figure 6A) in a dose-dependent manner. In contrast, ROS increased the mRNA expression levels of PAI-1, IL-6, and monocyte chemotactic protein-1 (MCP-1) in 3T3-L1 adipocytes
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15599400

Selventa

RAPsnww4zTncARGcDUnBPCslX B8NW8BOkLYbVw881rXc
has assertion: p(HGNC:CXCL10) => cat(p(HGNC:CXCR3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.445+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:CXCL10) => cat(p(HGNC:CXCR3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15602009

5
value: T cells in peripheral airways of COPD patients show increased expression of CXCR3, a receptor activated by interferon-{gamma} inducible protein of 10 kDa (IP-10; CXCL10), monokine induced by interferon-{gamma} (Mig; CXCL9), and interferon-inducible T cell-{alpha} chemoattractant (I-TAC; CXCL11). All three cytokines activate CXCR3, although CXCL11 has the highest affinity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15602009

Selventa

RAE95mg-zjVjb6S0YsCYJcFH9SV4pxdRtGVyRSxjU05Ic
has assertion: p(EGID:7295) -| kin(p(HGNC:MAP3K5))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.446+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(EGID:7295) -| kin(p(HGNC:MAP3K5))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15602009

5
value: Apoptosis signal-regulating kinase-1 (MAP3K5) is held in an inactive conformation by thioredoxin and when oxidized by ROS, this triggers the apoptotic pathway.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15602009

Selventa

RAI26RZve9CzqkuwJ4D3P5IEEsTkVyk8eeG55bhOC9ZB0
has assertion: a(CHEBI:"reactive oxygen species") -| r(MGI:Pon1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.464+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"reactive oxygen species") -| r(MGI:Pon1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15607899

3
value: PON1 expression is downregulated by oxidative stress. In contrast, more recent studies have shown that PON2 expression is upregulated in response to oxidative stress-inducing agents
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15607899

Selventa

RAOh3tNZXrbIqvv2e0Yv3bn6rOf0Pd-xe2tBvkq23WO Q
has assertion: bp(GO:"response to hypoxia") -> tscript(p(HGNC:TP53))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.466+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

bp(GO:"response to hypoxia") -> tscript(p(HGNC:TP53))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15607964

4
value: During hypoxia, Bnip3L is highly induced in wild-type p53-expressing cells, in part due to increased recruitment of p53 and CBP to Bnip3L.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15607964

Selventa

RANbUxAFg93sfQtqVLArU975Wpo0OifBZ3xra86ROfxF0
has assertion: cat(p(PFH:"HSP90 Family")) -> tscript(complex(NCH:"Nfkb Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.481+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(PFH:"HSP90 Family")) -> tscript(complex(NCH:"Nfkb Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15611262

5
value: Stress-induced transient insolubilization of the IkappaB kinase complex following its dissociation from Hsp90 represents a novel mechanism by which the activation of the stress response inhibits the NF-kappaB signaling pathway in response to proinflammatory stimuli.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15611262

Selventa

RAGaIeanMXKfN8Qs98qxsmcDkmHXUQiUkzNIPu0N0TCIE
has assertion: p(MGI:Tsc1) -| gtp(p(MGI:Rac1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.489+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Tsc1) -| gtp(p(MGI:Rac1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15611338

5
value: TSC1 inhibits Rac1, and TSC2 blocks this activity of TSC1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15611338

Selventa

RAGR88X4s15 KbJHIMrYdc6U-KAHLb3N4BdrDrk69zjto
has assertion: complex(p(MGI:Tsc1),p(MGI:Tsc2)) -| (p(MGI:Tsc1) -| gtp(p(MGI:Rac1)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.491+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Tsc1),p(MGI:Tsc2)) -| (p(MGI:Tsc1) -| gtp(p(MGI:Rac1)))
label: p(MGI:Tsc1) -| gtp(p(MGI:Rac1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15611338

Selventa

9
value: TSC1 inhibits Rac1, and TSC2 blocks this activity of TSC1.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15611338

RAHOKE-PWZ1H6PVCXxUTVnKroisOreZzCk NtRGvMucsw
has assertion: kin(p(PFH:"FGFR Family")) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.494+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFH:"FGFR Family")) -> kin(complex(NCH:"p85/p110 PI3Kinase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15613447

5
value: Activation of FGF receptors can activate multiple signal transduction pathways including the phospholipase Cgamma, phosphatidyl inositol 3-kinase, mitogen-activated protein kinase and signal transducers and activators of transcription (STAT) pathways
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15613447

Selventa

RAIV9e8MvnlEfz226YLBqqyrYM9SmUd8LTY4zSRT10lr4
has assertion: tscript(p(MGI:Foxa2)) -| r(MGI:Fasn)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.506+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -| r(MGI:Fasn)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15616563

5
value: Pharmacological intervention to inhibit phosphorylation of Foxa2 may be an effective treatment for type 2 diabetes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15616563

Selventa

RAE6sngnJWLNJxkYGdX0VcsnRwV2F-lupTemDUUj2Isqw
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Acox1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.514+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Acox1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15616563

5
value: Pharmacological intervention to inhibit phosphorylation of Foxa2 may be an effective treatment for type 2 diabetes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15616563

Selventa

RAPdbo6j1TBnf2xb85S35 KkhSkhahYQhyKzZKmU4TceY
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Decr2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.524+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Decr2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15616563

5
value: Pharmacological intervention to inhibit phosphorylation of Foxa2 may be an effective treatment for type 2 diabetes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15616563

Selventa

RAK0erpdfNHjKDioVRXiScpl01VbrwumgiQoyjI9r8Bnw
has assertion: tscript(p(MGI:Foxa2)) -> r(MGI:Lipg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.532+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(MGI:Foxa2)) -> r(MGI:Lipg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15616563

5
value: Pharmacological intervention to inhibit phosphorylation of Foxa2 may be an effective treatment for type 2 diabetes.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15616563

Selventa

RAPM ml20FMLBlpCXAPDUlEDVv9fYmRdIp6tsr6k5IySw
has assertion: gtp(p(PFH:"RAS Family")) -> bp(GO:"DNA methylation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.562+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

gtp(p(PFH:"RAS Family")) -> bp(GO:"DNA methylation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15618232

4
value: We tested the hypothesis that up-regulation of DNA methyltransferase 1 (DNMT1) will lead to methylation and silencing of uPA and inhibition of the invasiveness of metastatic breast cancer cells. Since RAS was previously shown to up-regulate DNA methylation, we examined the effects of ectopic expression of constitutively active RAS on methylation and expression of uPA.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15618232

Selventa

RAFG2jJE6DIzpOrx7GecfRpRwfi4exlmg3aGT-vGe8E0I
has assertion: a(SCHEM:Acetaminophen) -> r(MGI:Igfbp1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.568+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:Acetaminophen) -> r(MGI:Igfbp1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15618236

3
value: Table II. Changes in expression in liver determined by QRT-PCR after treatment for 2 weeks with different known carcinogens and non-carcinogens
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15618236

Selventa

RAJcNCXeHLGSfsm4vUXkEEzKfbUR6NWq AOaWUZUmXWyo
has assertion: p(HGNC:S1PR1) -> r(HGNC:ANGPT1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.570+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:S1PR1) -> r(HGNC:ANGPT1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15618544

4
value: INTERPRETED FROM TEXT: Genes downregulated by stable sphingosine 1-phosphate knockdown in an angiosarcoma cell line using Affymetrix Human Genome U133A GeneChips.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15618544

Selventa

RAHqBTT1T2aI 7kCyxtJT4W1oZO1ZKY263jZYyVItPzOE
has assertion: p(HGNC:S1PR1) -> r(HGNC:PROCR)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.585+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:S1PR1) -> r(HGNC:PROCR)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15618544

4
value: INTERPRETED FROM TEXT: Genes downregulated by stable sphingosine 1-phosphate knockdown in an angiosarcoma cell line using Affymetrix Human Genome U133A GeneChips.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15618544

Selventa

RAEXezu3okoN2cxxhFFkh-6tXavAJixkoFGm6zORS8ZKk
has assertion: tscript(p(HGNC:SMAD3)) -> complex(p(HGNC:CREBBP),p(HGNC:SOX9))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.597+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tscript(p(HGNC:SMAD3)) -> complex(p(HGNC:CREBBP),p(HGNC:SOX9))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15623506

7
value: Interestingly, the association between Sox9 and CBP/p300 was increased by Smad3 overexpression and was suppressed by si-Smad3
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15623506

Selventa

RAGQFuOc1Xk0C5c4KLYU5FT0mgIVCTbSwMRrJ4nft8PLQ
has assertion: complex(p(MGI:Lum),p(MGI:Fasl)) => cat(p(MGI:Fas))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.611+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:Lum),p(MGI:Fasl)) => cat(p(MGI:Fas))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15623759

7
value: The data suggest that lumican binds FasL and facilitates induction of Fas.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15623759

Selventa

RAJu8h5ohM5o3e28F-xv0p zTmphjOp71KHD3Muv1XoX4
has assertion: a(CHEBI:biotin) -> r(HGNC:MCCC1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.618+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:biotin) -> r(HGNC:MCCC1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15623830

3
value: RT-PCR at d 0 and 28. At d 28, SLC19A3 expression had decreased to 33% of d 0 (P < 0.02 by two-tailed, paired t test). Expression of MCCA, PCCA, PC, ACCA, ACCB, HCS, biotinidase, and SMVT decreased to approximately 80% of d 0 (P < 0.05).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15623830

Selventa

RAFlhE24vi HVlmrpP4byMLcHzozLRRTyAGrhqvvAlrT4
has assertion: a(CHEBI:biotin) -> r(HGNC:PC)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.619+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:biotin) -> r(HGNC:PC)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15623830

3
value: RT-PCR at d 0 and 28. At d 28, SLC19A3 expression had decreased to 33% of d 0 (P < 0.02 by two-tailed, paired t test). Expression of MCCA, PCCA, PC, ACCA, ACCB, HCS, biotinidase, and SMVT decreased to approximately 80% of d 0 (P < 0.05).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15623830

Selventa

RAIt0 FHX54UuwdhUxcQdOeSgWDHqN7lj3T3udv7wGuyg
has assertion: a(CHEBI:biotin) -> r(HGNC:PCCA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.620+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:biotin) -> r(HGNC:PCCA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15623830

3
value: RT-PCR at d 0 and 28. At d 28, SLC19A3 expression had decreased to 33% of d 0 (P < 0.02 by two-tailed, paired t test). Expression of MCCA, PCCA, PC, ACCA, ACCB, HCS, biotinidase, and SMVT decreased to approximately 80% of d 0 (P < 0.05).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15623830

Selventa

RAPEd1iU0htkEsxeUwLHcYthlY84KrWzGr4eZgPUXZofg
has assertion: a(CHEBI:"hyaluronic acid") -> bp(GO:"cellular extravasation")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.623+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:"hyaluronic acid") -> bp(GO:"cellular extravasation")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15624323

2
value: The extracellular matrix glycosaminoglycan hyaluronan (HA)1 is a large polymer of N-acetyl-D-glucosamine and D-glucuronic acid (molecular mass 105-107 Da) which plays an important role in maintaining tissue integrity as well as facilitating the migration of cells during inflammation, wound repair, and embryonic development (1, 2).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15624323

Selventa

RAKu3Gdd5pl9XR3yF TvrEKhUliW6-LFp Pl0qrhII TI
has assertion: cat(p(MGI:Itgb1)) -> kin(p(MGI:Ptk2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.634+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(MGI:Itgb1)) -> kin(p(MGI:Ptk2))
label: p(MGI:Slc3a2) -> (cat(p(MGI:Itgb1)) -> kin(p(MGI:Ptk2)))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15625115

8
value: beta1 integrins play an important role in cell proliferation and in some cancers and we report here that CD98hc enhances beta1 activation of signaling pathways such as FAK, Rac and Akt
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15625115

Selventa

RALTUuAuAKlKrQEfL8WCZhtkdFnnLYnpuu7Whd NDwx7Y
has assertion: kin(p(PFR:"Akt Family")) -> r(RGD:Apoe)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.642+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(p(PFR:"Akt Family")) -> r(RGD:Apoe)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15627653

5
value: Differential inhibition of signaling pathways suggested that FGF-1 stimulates apoE synthesis via the phosphoinositide 3-OH kinase for PI3K/Akt pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15627653

Selventa

RAISsFw4HmLvk5wUEMU3ZSJ urCkZSnbfauqcuyfYGNeg
has assertion: kin(complex(NCR:"p85/p110 PI3Kinase Complex")) -> r(RGD:Apoe)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.643+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

kin(complex(NCR:"p85/p110 PI3Kinase Complex")) -> r(RGD:Apoe)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15627653

4
value: Differential inhibition of signaling pathways suggested that FGF-1 stimulates apoE synthesis via the phosphoinositide 3-OH kinase for PI3K/Akt pathway
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15627653

Selventa

RANVAc9dJqsge2WKTqg5X6NtVv DUmb8S2hOIlvyEvCCw
has assertion: p(HGNC:TGFB1) -| a(CHEBI:glutathione)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.653+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:TGFB1) -| a(CHEBI:glutathione)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15629866

3
value: TGF-beta suppression of the Phase II genes correlated with a decrease in cellular glutathione and an increase in cellular reactive oxygen species
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15629866

Selventa

RAKb-2xIA bZpWbAgwCq2hDo62VqR-UtBFLghlYh70qdc
has assertion: cat(p(HGNC:HRH1)) -> cat(p(EGID:115557))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.660+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:HRH1)) -> cat(p(EGID:115557))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15632174

6
value: Here we report that p63RhoGEF, a recently identified RhoA-specific guanine nucleotide exchange factor, enhances the Rho-dependent gene transcription induced by agonist-stimulated G(q/11)-coupled receptors (M3-cholinoceptor, histamine H1 receptor) or GTPase-deficient mutants of G alpha(q) and G alpha11.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15632174

Selventa

RAEMS9rZmMpZ7Ur0N47nsKcuTlghit3CMWVS zLd0LEbc
has assertion: p(MGI:Il4) -| phos(p(MGI:Ppp1ca))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.671+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Il4) -| phos(p(MGI:Ppp1ca))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15634756

5
value: consequence of an intracellular signal triggered by interleukin-4 deprivation. Growth factor deprivation in turn induces PP1alpha phosphatase activation
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15634756

Selventa

RANKslCnQsWBYPtfbMZNSM Dh KyavZm9DX1p52yzX WY
has assertion: phos(p(MGI:Ppp1ca)) -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.672+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

phos(p(MGI:Ppp1ca)) -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15634756

4
value: translocation of Bad from rafts to mitochondria, which correlates with apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15634756

Selventa

RAPeP1XNFD rZ9yIjjJyRpxIJ2iD5vNx1AbrWHGLyo-mw
has assertion: tloc(p(MGI:Casp3),GOCCACC:"GO:0005737",GOCCACC:"GO:0005886") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.674+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(MGI:Casp3),GOCCACC:"GO:0005737",GOCCACC:"GO:0005886") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15634756

4
value: translocation of Bad from rafts to mitochondria, which correlates with apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15634756

Selventa

RANNKh6cxW047U9t-gPOZAtdShZ IWvlnqr6OI4Z2gjmM
has assertion: tloc(p(MGI:Casp9),GOCCACC:"GO:0005737",GOCCACC:"GO:0005886") -> bp(MESHPP:Apoptosis)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.675+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

tloc(p(MGI:Casp9),GOCCACC:"GO:0005737",GOCCACC:"GO:0005886") -> bp(MESHPP:Apoptosis)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15634756

4
value: translocation of Bad from rafts to mitochondria, which correlates with apoptosis
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15634756

Selventa

RAGNmQev0uea0DCSWkeD9WNyE5PTKHskWMmUhTSdssBs0
has assertion: a(CHEBI:estradiol) -> r(HGNC:AP1B1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.682+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:AP1B1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Examples of genes whose expression was increased or decreased by E2 are provided in Tables 3 and 4, respectively. TABLE 3. Examples of genes up-regulated by E2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAFah5JoMpYZcLX-qvqH Rsw7oHNpe2aNLYrR8k7WSlJg
has assertion: a(CHEBI:estradiol) -> r(HGNC:IL1RN)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.690+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:IL1RN)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Examples of genes whose expression was increased or decreased by E2 are provided in Tables 3 and 4, respectively. TABLE 3. Examples of genes up-regulated by E2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAMhBAGjrESgRSLj8v YqykQj7IF4O7D1IJ2jzz4cQA8w
has assertion: a(CHEBI:estradiol) -> r(HGNC:PPP1CA)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.697+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:PPP1CA)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Examples of genes whose expression was increased or decreased by E2 are provided in Tables 3 and 4, respectively. TABLE 3. Examples of genes up-regulated by E2
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAPFLd28cbXLb-XYJiMse1U6qqMUh15LV1iAAStxDFRKg
has assertion: a(CHEBI:estradiol) -> r(HGNC:KPNA1)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.722+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:KPNA1)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Table 5. genes upregulated by estrogen in MCF-7 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAEWMVrwzPW1g-to5aHsSfGpB3obwP9A6a3pN JDkEpPg
has assertion: a(CHEBI:estradiol) -> r(HGNC:RLN2)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.725+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:RLN2)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Table 5. genes upregulated by estrogen in MCF-7 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAJyeE3EYAvOmadraHI9Q9TXEtU2g9URvi5e05fYB1CME
has assertion: a(CHEBI:estradiol) -> r(HGNC:TFF3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.726+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -> r(HGNC:TFF3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Table 5. genes upregulated by estrogen in MCF-7 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAIrN5A7kgdpN4YWG4MhoiYtSK8naD6a1UWM3 pkb8-FE
has assertion: a(CHEBI:estradiol) -| r(HGNC:KCNJ8)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.774+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -| r(HGNC:KCNJ8)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Table 6. genes downregulated by estrogen in MCF-7 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAF37ASJcgQL6ljxzJLbHdG3n7j0mAA3 lrx9F1of2Sak
has assertion: a(CHEBI:estradiol) -| r(HGNC:NCOA3)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.778+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(CHEBI:estradiol) -| r(HGNC:NCOA3)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15637295

3
value: Table 6. genes downregulated by estrogen in MCF-7 cells
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15637295

Selventa

RAFfZL3H4Ni5dzNzCSTYEK3cnMdNlkfsSpIGidRjzPWy4
has assertion: a(SCHEM:"8-Isoprostane") -> kin(p(PFH:"MAPK JNK Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.783+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

a(SCHEM:"8-Isoprostane") -> kin(p(PFH:"MAPK JNK Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15640282

4
value: Signal transduction pathway inhibitors (SB203580, curcumin, and PD98059) implicated p38 and JNK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15640282

Selventa

RAHlSNKiO9a5U1RRFoNEteOfDgIBbtjDi-Tza0wntmnsE
has assertion: cat(p(HGNC:TBXA2R)) -> kin(p(PFH:"MAPK JNK Family"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.786+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:TBXA2R)) -> kin(p(PFH:"MAPK JNK Family"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15640282

6
value: Signal transduction pathway inhibitors (SB203580, curcumin, and PD98059) implicated p38 and JNK
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15640282

Selventa

RAIpEfl vR18MwYhtv--iVeR-aYUS0NMYDIv4FBSLGeuA
has assertion: complex(p(MGI:S100a8),p(MGI:S100a9),a(CHEBI:"arachidonic acid")) -> cat(complex(NCM:"NADPH Oxidase Complex"))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.795+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(MGI:S100a8),p(MGI:S100a9),a(CHEBI:"arachidonic acid")) -> cat(complex(NCM:"NADPH Oxidase Complex"))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15642721

6
value: Moreover, S100A8/A9 transferred the cofactor arachidonic acid to NADPH oxidase as shown by the impotence of a mutant S100A8/A9 complex unable to bind arachidonic acid to enhance NADPH oxidase activity.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15642721

Selventa

RAOGAzvwE6feRG6VoCnAATBCB1eng5Lz-VVlu9ruxPowQ
has assertion: p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapk14)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.807+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapk14)))
label: p(PFM:"Ifna Family") -> kin(p(MGI:Mapk14))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

7
value: IFN-dependent activation of the downstream effectors of p38, MAPKAPK-2 and MAPKAPK-3, is not detectable in cells lacking Mkk3 and Mkk6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RALTuAF5hR5DDVlzfEqPNAD-fGNZXK3a9LLj YhECyJJ8
has assertion: p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.810+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2)))
label: p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

7
value: IFN-dependent activation of the downstream effectors of p38, MAPKAPK-2 and MAPKAPK-3, is not detectable in cells lacking Mkk3 and Mkk6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RANwZo-WrnJ7QTEzCjXAqphYcNpfTk53Gt0GhlDJW0QtQ
has assertion: p(MGI:Map2k6) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2)))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.818+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Map2k6) -> (p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2)))
label: p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

7
value: IFN-dependent activation of the downstream effectors of p38, MAPKAPK-2 and MAPKAPK-3, is not detectable in cells lacking Mkk3 and Mkk6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RALDIczzgYozpFIrDDCV84la16Dfes9rtl2DWCIlcDGV8
has assertion: p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.823+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

5
value: IFN-dependent activation of the downstream effectors of p38, MAPKAPK-2 and MAPKAPK-3, is not detectable in cells lacking Mkk3 and Mkk6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RANvn7LKurq2fP-Wby-jETjj80xky1jeEkb2rHoYcrJ5Y
has assertion: p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.824+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFM:"Ifna Family") -> kin(p(MGI:Mapkapk2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

5
value: IFN-dependent activation of the downstream effectors of p38, MAPKAPK-2 and MAPKAPK-3, is not detectable in cells lacking Mkk3 and Mkk6
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RAN844CQG076Si7cOu7t1IPK4HvBj3DhWF9uxZtm0S8pY
has assertion: p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> r(MGI:Irf9))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.832+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Map2k3) -> (p(PFM:"Ifna Family") -> r(MGI:Irf9))
label: p(PFM:"Ifna Family") -> r(MGI:Irf9)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

6
value: IFN-dependent induction of two genes known to be of importance in the generation of IFN responses, Isg15 and Irf-9, was diminished in the absence of Mkk3 and Mkk6.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RAEaViAi3kEvyCq7N2zO2CCO8VMOT6e3-GeZEvA3u5K-Y
has assertion: p(PFM:"Ifna Family") -> kin(p(MGI:Map2k6))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.848+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(PFM:"Ifna Family") -> kin(p(MGI:Map2k6))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15644321

5
value: IFNalpha- and IFNbeta-dependent transcription via either interferon-stimulated response element or IFNgamma activated site elements was defective in MKK3 -/-/MKK6 -/- MEFs
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15644321

Selventa

RANEJ4jBprANwPcpeCGBtsqQh lWkrFL THCWV22o1Tsw
has assertion: complex(p(HGNC:IHH),p(HGNC:PTCH1)) -> tscript(p(HGNC:GLI1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.865+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:IHH),p(HGNC:PTCH1)) -> tscript(p(HGNC:GLI1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15645142

7
value: Sonic hedgehog (SHH), Desert hedgehog (DHH) and Indian hedgehog (IHH) bind to Patched family receptors (PTCH1 and PTCH2) to transduce signals to GLI1, GLI2 and GLI3. GLI family transcription factors then activate transcription of Hedgehog target genes, such as FOXE1 and FOXM1 encoding Forkhead-box transcription factors.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15645142

Selventa

RAIq8mmL0uY0LxUNKn1pIfb8ZSxD9nMCXxKdoUyElrUFU
has assertion: complex(p(HGNC:SHH),p(HGNC:PTCH1)) -> tscript(p(HGNC:GLI2))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.869+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:SHH),p(HGNC:PTCH1)) -> tscript(p(HGNC:GLI2))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15645142

7
value: Sonic hedgehog (SHH), Desert hedgehog (DHH) and Indian hedgehog (IHH) bind to Patched family receptors (PTCH1 and PTCH2) to transduce signals to GLI1, GLI2 and GLI3. GLI family transcription factors then activate transcription of Hedgehog target genes, such as FOXE1 and FOXM1 encoding Forkhead-box transcription factors.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15645142

Selventa

RAMb PEkk lAfD9fhhbFEMBxrUW12FGDah4YJyyB 2pXA
has assertion: complex(p(HGNC:SHH),p(HGNC:PTCH2)) -> tscript(p(HGNC:GLI1))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.873+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

complex(p(HGNC:SHH),p(HGNC:PTCH2)) -> tscript(p(HGNC:GLI1))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15645142

7
value: Sonic hedgehog (SHH), Desert hedgehog (DHH) and Indian hedgehog (IHH) bind to Patched family receptors (PTCH1 and PTCH2) to transduce signals to GLI1, GLI2 and GLI3. GLI family transcription factors then activate transcription of Hedgehog target genes, such as FOXE1 and FOXM1 encoding Forkhead-box transcription factors.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15645142

Selventa

RALLjOkukUC5Lbvuxqpri4iJNZCiai-niVdcEP-rnwfUA
has assertion: p(MGI:Tgfb1) -> bp(GO:"actin filament polymerization")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.895+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(MGI:Tgfb1) -> bp(GO:"actin filament polymerization")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15647284

3
value: TGF-beta1 induced rapid actin polymerization into stress fibers and concomitantly activated RhoA and RhoB small GTPases.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15647284

Selventa

RANw-Wn873ictFffxZSX69rVpRCWYiMsLQtu1XlIirDQs
has assertion: cat(p(HGNC:BMP2)) -> complex(p(HGNC:ITGAV),p(HGNC:ITGB3))
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.899+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

cat(p(HGNC:BMP2)) -> complex(p(HGNC:ITGAV),p(HGNC:ITGB3))
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15647827

7
value: Human osteoblasts (HOBs) express alphabeta1, alphavbeta3, alphavbeta5, alphavbeta6, and alphavbeta8 integrins at focal adhesion sites. BMP-2 increases the levels of these integrins on osteoblast surface
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15647827

Selventa

RAGcA8I5L9zUHsuCQpoP13d5lPpm8OtOV1X3jO74nQjr4
has assertion: path(SDIS:castration) -> r(MGI:Areg)
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.920+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

path(SDIS:castration) -> r(MGI:Areg)
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15651060

3
value: A fraction of growth factors showed a steady increase in the mRNA expression reaching between fourfold and eightfold 30 days after castration, including amphiregulin (P < 0.005) and epiregulin (P < 0.001).
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15651060

Selventa

RAKud7yp5nPdrCfTf46EOMh4gS9XFnovzjR07-g1Ow3HA
has assertion: p(HGNC:IFNB1) -> p(HGNC:"HLA-G")
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.925+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234

p(HGNC:IFNB1) -> p(HGNC:"HLA-G")
had primary source: http://www.ncbi.nlm.nih.gov/pubmed/15652415

4
value: Although both IFN-beta and IFN-gamma strongly enhance HLA-G1 and HLA-G5 expression by monocytes in vitro, IFN-beta leads to a stronger relative upregulation of HLA-G compared to classical MHC class I molecules than stimulation with IFN-gamma.
was quoted from: http://www.ncbi.nlm.nih.gov/pubmed/15652415

Selventa

RAHxqiOwGRBnfLuA8GrinOLzJIuxKWSm4sXn0jPUeEfnI
has assertion: assertion
has provenance: provenance
has publication info: pubinfo
type: Nanopublication
created: 2014-07-03T14:30:30.930+02:00
created by: 0000-0001-6818-334X
created by: http://orcid.org/0000-0002-1267-0234