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All rights reserved." } ], "http://purl.org/dc/elements/1.1/title" : [ { "@value" : "BEL Framework Large Corpus Document" } ], "http://purl.org/pav/authoredBy" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_4" } ], "http://purl.org/pav/version" : [ { "@value" : "20131211" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_3", "http://www.w3.org/ns/prov#value" : [ { "@value" : "Tumor necrosis factor-alpha (TNF-alpha) is a potent inducer of insulin resistance, and increased TNF-alpha expression is associated with impaired glucose disposal. Although insulin is the primary regulator of glucose transport in adipose, endothelin-1, a vasoconstrictor peptide that signals through the heterotrimeric G proteins Galphaq/11, potently stimulates glucose uptake in 3T3-L1 adipocytes by a mechanism independent of phosphatidylinositol (PI) 3-kinase. 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