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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_3 http://www.w3.org/ns/prov#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. Here, we report that exposure of 3T3-L1 adipocytes to TNF-alpha for 48 h dose-dependently decreased endothelin-1-stimulated glucose uptake and translocation of GLUT4 to the plasma membrane. TNF-alpha exposure had no effect on endothelin-1 receptor number at the cell surface. In contrast, TNF-alpha treatment reduced the quantity of Galphaq/11 and proline-rich tyrosine kinase 2 (PYK2) and decreased endothelin-1-stimulated PYK2-Tyr402 tyrosine phosphorylation. Taken together, these results suggest that TNF-alpha-induced desensitization of endothelin-1-stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes is due, at least in part, to a decreased expression of Galphaq/11, leading to a suppression in tyrosine phosphorylation of PYK2. http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_3 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/12773307 http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_4 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/12773307 http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#_3 http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic#pubinfo http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic http://purl.org/dc/terms/created 2014-07-03T14:32:02.600+02:00 http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RAV3LXFzp1Wg3bwLON0_VKRv-BkcBAJCrEr78X0J3_Sic http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234