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dc.contributor.authorArribas, Mónica-
dc.contributor.authorValverde, Ángela M.-
dc.contributor.authorBurks, Deborah J.-
dc.contributor.authorBenito, Manuel-
dc.date.accessioned2017-07-07T12:04:50Z-
dc.date.available2017-07-07T12:04:50Z-
dc.date.issued2003-
dc.identifierdoi: 10.1016/S0014-5793(03)00049-8-
dc.identifierissn: 0014-5793-
dc.identifiere-issn: 1873-3468-
dc.identifier.citationFEBS Letters 536(1-3): 161-166 (2003)-
dc.identifier.urihttp://hdl.handle.net/10261/152501-
dc.description.abstractInsulin receptor substrate-2-deficient (IRS-2-/-) mice develop type 2 diabetes. We have investigated the molecular mechanisms by which IRS-2-/- immortalized brown adipocytes showed an impaired response to insulin in inducing GLUT4 translocation and glucose uptake. IRS-2-associated phosphatidylinositol 3-kinase (PI 3-kinase) activity was blunted in IRS-2-/- cells, total PI 3-kinase activity being reduced by 30%. Downstream, activation of protein kinase C (PKC) ζ was abolished in IRS-2-/- cells. Reconstitution with retroviral IRS-2 restores IRS-2/PI 3-kinase/PKCζ signalling, as well as glucose uptake. Wild-type cells expressing a kinase-inactive mutant of PKCζ lack GLUT4 translocation and glucose uptake. Our results support the essential role played by PKCζ in the insulin resistance and impaired glucose uptake observed in IRS-2-deficient brown adipocytes.-
dc.description.sponsorshipThis work was supported by Grant SAF2001/1302 from M.C.T., Spain.-
dc.publisherElsevier-
dc.rightsclosedAccess-
dc.subjectInsulin receptor substrate-2-
dc.subjectGlucose transport-
dc.subjectProtein kinase C-
dc.titleEssential role of protein kinase Cζ in the impairment of insulin-induced glucose transport in IRS-2-deficient brown adipocytes-
dc.typeartículo-
dc.identifier.doi10.1016/S0014-5793(03)00049-8-
dc.date.updated2017-07-07T12:04:50Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderMinisterio de Ciencia y Tecnología (España)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100006280es_ES
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