pubmed-article:15581361 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0206131 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1418576 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1418577 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1423080 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1423613 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1167622 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0178666 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:15581361 | lifeskim:mentions | umls-concept:C0758621 | lld:lifeskim |
pubmed-article:15581361 | pubmed:issue | 49 | lld:pubmed |
pubmed-article:15581361 | pubmed:dateCreated | 2004-12-7 | lld:pubmed |
pubmed-article:15581361 | pubmed:abstractText | Cbl is phosphorylated by the insulin receptor and reportedly functions within the flotillin/CAP/Cbl/Crk/C3G/TC10 complex during insulin-stimulated glucose transport in 3T3/L1 adipocytes. Cbl, via pYXXM motifs at tyrosine-371 and tyrosine-731, also activates phosphatidylinositol (PI) 3-kinase, which is required to activate atypical protein kinase C (aPKC) and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes [Miura et al. (2003) Biochemistry 42, 14335-14341]. Presently, we have examined the importance of Cbl in activating PI 3-kinase and aPKC during insulin action in 3T3/L1 adipocytes by expressing Y371F and Y731F Cbl mutants, which nullify pYXXM binding of Cbl to SH2 domains of downstream effectors. Interestingly, these mutants inhibited insulin-induced increases in (a) binding of Cbl to both Crk and the p85 subunit of PI 3-kinase, (b) activation of Cbl-dependent PI 3-kinase, (c) activation and translocation of aPKC to the plasma membrane, (d) translocation of Glut4 to the plasma membrane, (e) and glucose transport. Importantly, coexpression of wild-type Cbl reversed the inhibitory effects of Cbl mutants. In contrast to Cbl-dependent PI 3-kinase, Cbl mutants did not significantly inhibit the activation of PI 3-kinase by IRS-1, which is also required during insulin action. Our findings suggest that (a) Cbl uses pYXXM motifs to simultaneously activate PI 3-kinase and Crk/C3G/TC10 pathways and (b) Cbl, along with IRS-1, functions upstream of PI 3-kinase and aPKCs during insulin-stimulated glucose transport in 3T3/L1 adipocytes. | lld:pubmed |
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pubmed-article:15581361 | pubmed:language | eng | lld:pubmed |
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pubmed-article:15581361 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15581361 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15581361 | pubmed:month | Dec | lld:pubmed |
pubmed-article:15581361 | pubmed:issn | 0006-2960 | lld:pubmed |
pubmed-article:15581361 | pubmed:author | pubmed-author:Bandyopadhyay... | lld:pubmed |
pubmed-article:15581361 | pubmed:author | pubmed-author:SajanMini PMP | lld:pubmed |
pubmed-article:15581361 | pubmed:author | pubmed-author:StandaertMary... | lld:pubmed |
pubmed-article:15581361 | pubmed:author | pubmed-author:FareseRobert... | lld:pubmed |
pubmed-article:15581361 | pubmed:author | pubmed-author:MiuraAtsushiA | lld:pubmed |
pubmed-article:15581361 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15581361 | pubmed:day | 14 | lld:pubmed |
pubmed-article:15581361 | pubmed:volume | 43 | lld:pubmed |
pubmed-article:15581361 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15581361 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15581361 | pubmed:pagination | 15494-502 | lld:pubmed |
pubmed-article:15581361 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:15581361 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15581361 | pubmed:articleTitle | Requirements for pYXXM motifs in Cbl for binding to the p85 subunit of phosphatidylinositol 3-kinase and Crk, and activation of atypical protein kinase C and glucose transport during insulin action in 3T3/L1 adipocytes. | lld:pubmed |
pubmed-article:15581361 | pubmed:affiliation | Research Service, James A. Haley Veterans Medical Center, and Department of Internal Medicine, University of South Florida College of Medicine, Tampa, Florida 33612, USA. | lld:pubmed |
pubmed-article:15581361 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15581361 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:15581361 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:15581361 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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