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http://amigo.geneontology.org/amigo/term/GO:0043234
http://www.tkuhn.ch/bel2nanopub/RAokXc7GjNaUnBPrKXzzEbwuhY_p1Wcp0RihdBokOFaqU#_1
http://semanticscience.org/resource/SIO_000139
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http://resource.belframework.org/belframework/1.0/namespace/selventa-legacy-diseases/muscle%20glucose%20import
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http://purl.obolibrary.org/obo/BFO_0000066
http://purl.bioontology.org/ontology/MSH/D009130
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a(SCHEM:"serum insulin") -> path(SDIS:"muscle glucose import")
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http://www.w3.org/2000/01/rdf-schema#label
kin(complex(NCH:"p85/p110 PI3Kinase Complex")) -> (a(SCHEM:"serum insulin") -> path(SDIS:"muscle glucose import"))
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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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Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin
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http://www.w3.org/ns/prov#wasQuotedFrom
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Selventa
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2014-07-03T14:29:46.521+02:00
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