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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAaKHohI3DPx5IU-z2R4Te_3eI_aQso_tEau6_nkR3Zho#_1
http://purl.obolibrary.org/obo/RO_0002204
http://rgd.mcw.edu/rgdweb/report/gene/main.html?id=628748
http://www.tkuhn.ch/bel2nanopub/RAaKHohI3DPx5IU-z2R4Te_3eI_aQso_tEau6_nkR3Zho#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://purl.obolibrary.org/obo/BFO_0000066
http://purl.obolibrary.org/obo/UBERON_0002107
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http://purl.obolibrary.org/obo/BFO_0000066
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-chemicals/serum%20fatty%20acid
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http://www.w3.org/1999/02/22-rdf-syntax-ns#predicate
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http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
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http://www.w3.org/2000/01/rdf-schema#label
p(RGD:Adipoq) -| a(SCHEM:"serum fatty acid")
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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http://www.w3.org/ns/prov#value
In addition, we (12) and others (13,14) have previously demonstrated that TNF-A represses the mRNA levels of an adipocyte-derived hormone, ACRP30, which inhibits gluconeogenesis in the liver (15), and decreases plasma levels of glucose (16) and FFAs (17). Thus, the increased circulating FFA concentrations and/or reduced ACRP30 protein levels could mediate some of the delayed effects of TNF-A on whole-body energy metabolism.
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/12401708
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
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http://www.w3.org/ns/prov#wasDerivedFrom
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http://purl.org/dc/terms/created
2014-07-03T14:31:55.882+02:00
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