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http://www.tkuhn.ch/bel2nanopub/RAgoGfDxwXcS6C2n6oF_JExnIxcRZU7vW6HTs-pahi5yM#_1
http://semanticscience.org/resource/SIO_000139
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http://amigo.geneontology.org/amigo/term/GO:0016301
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http://purl.obolibrary.org/obo/RO_0002204
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kin(p(HGNC:MAPK1)) -> p(HGNC:PPARG,pmod(P))
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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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1.4
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As might be expected from the wide array of hormones, cytokines, and growth factors that can affect adipogenesis, several different signal transduction pathways have been implicated in the process as well. There has been quite a bit of interest in the MAP kinase family of intracellular protein kinases. As just described, many growth factors that exert their influence through tyrosine kinase receptors inhibit fat cell differentiation. It is now clear that much of this inhibition occurs through activation of the \"classic\" MAP kinases, Erk 1 and 2. These kinases directly phosphorylate PPARg (see subsequent text), and inhibit its adipogenic activity.33
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http://www.w3.org/ns/prov#wasQuotedFrom
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Selventa
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http://www.w3.org/ns/prov#wasDerivedFrom
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2014-07-03T14:30:09.556+02:00
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