http://purl.uniprot.org/citations/23640896 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23640896 | http://www.w3.org/2000/01/rdf-schema#comment | "Insulin activates a cascade of signaling molecules, including Rac-1, Akt, and AS160, to promote the net gain of glucose transporter 4 (GLUT4) at the plasma membrane of muscle cells. Interestingly, constitutively active Rac-1 expression results in a hormone-independent increase in surface GLUT4; however, the molecular mechanism and significance behind this effect remain unresolved. Using L6 myoblasts stably expressing myc-tagged GLUT4, we found that overexpression of constitutively active but not wild-type Rac-1 sufficed to drive GLUT4 translocation to the membrane of comparable magnitude with that elicited by insulin. Stimulation of endogenous Rac-1 by Tiam1 overexpression elicited a similar hormone-independent gain in surface GLUT4. This effect on GLUT4 traffic could also be reproduced by acutely activating a Rac-1 construct via rapamycin-mediated heterodimerization. Strategies triggering Rac-1 "superactivation" (i.e. to levels above those attained by insulin alone) produced a modest gain in plasma membrane phosphatidylinositol 3,4,5-trisphosphate, moderate Akt activation, and substantial AS160 phosphorylation, which translated into GLUT4 translocation and negated the requirement for IRS-1. This unique signaling capacity exerted by Rac-1 superactivation bypassed the defects imposed by JNK- and ceramide-induced insulin resistance and allowed full and partial restoration of the GLUT4 translocation response, respectively. We propose that potent elevation of Rac-1 activation alone suffices to drive insulin-independent GLUT4 translocation in muscle cells, and such a strategy might be exploited to bypass signaling defects during insulin resistance."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m113.467647"xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/author | "Sun Y."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/author | "Klip A."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/author | "Chiu T.T."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/author | "Koshkina A."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/pages | "17520-17531"xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/title | "Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance."xsd:string |
http://purl.uniprot.org/citations/23640896 | http://purl.uniprot.org/core/volume | "288"xsd:string |
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