| pubmed-article:9572482 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0015350 | lld:lifeskim |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:9572482 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:9572482 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9572482 | pubmed:dateCreated | 1998-5-15 | lld:pubmed |
| pubmed-article:9572482 | pubmed:abstractText | When 3T3-L1 preadipose cells are exposed to transforming growth factor beta (TGFbeta), they synthesize more extracellular matrix (ECM) and resist differentiation-inducing stimuli. The mechanism by which ECM suppresses adipose cell differentiation (adipogenesis) remains unknown. Since adipogenesis is an insulin/insulin-like growth factor-1 (IGF-1)-dependent process, we investigated whether TGFbeta-induced ECM inhibits insulin signaling. When preadipose cells were pretreated overnight with TGFbeta, we observed a 75% decrease in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) compared to that in control cells. Culturing 3T3-L1 preadipose cells on fibronectin, a component of the ECM induced by TGFbeta, also inhibited insulin-dependent IRS-1 tyrosine phosphorylation and adipogenesis, supporting a role for ECM in mediating TGFbeta's inhibitory effect on insulin signaling. Since the insulin-stimulated association of phosphoinositide (PI) 3-kinase with IRS-1 depends on IRS-1 tyrosine phosphorylation, we measured the presence of the PI 3-kinase 85 kDa regulatory subunit in anti-IRS-1 immunoprecipitates. Following insulin stimulation, PI 3-kinase-IRS-1 association was reduced by 70% in TGFbeta pretreated vs. control preadipose cells. However, insulin-stimulated cellular production of PI(3,4,5)P3 was unaltered by TGFbeta pretreatment. This suggests that IRS-1-associated p85-type PI 3-kinase may represent a particular subset of total cellular PI 3-kinase that is specifically inhibited by TGFbeta. Reduction of insulin-stimulated association of IRS-1 with p85-type PI 3-kinase by TGFbeta may be one potential mechanism through which TGFbeta blocks 3T3-L1 adipose cell differentiation. | lld:pubmed |
| pubmed-article:9572482 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9572482 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9572482 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9572482 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:9572482 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:9572482 | pubmed:author | pubmed-author:ChabotJJ | lld:pubmed |
| pubmed-article:9572482 | pubmed:author | pubmed-author:GagnonA MAM | lld:pubmed |
| pubmed-article:9572482 | pubmed:author | pubmed-author:SoriskyAA | lld:pubmed |
| pubmed-article:9572482 | pubmed:author | pubmed-author:PardasaniDD | lld:pubmed |
| pubmed-article:9572482 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9572482 | pubmed:volume | 175 | lld:pubmed |
| pubmed-article:9572482 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9572482 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9572482 | pubmed:pagination | 370-8 | lld:pubmed |
| pubmed-article:9572482 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9572482 | pubmed:meshHeading | pubmed-meshheading:9572482-... | lld:pubmed |
| pubmed-article:9572482 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9572482 | pubmed:articleTitle | Extracellular matrix induced by TGFbeta impairs insulin signal transduction in 3T3-L1 preadipose cells. | lld:pubmed |
| pubmed-article:9572482 | pubmed:affiliation | Ottawa Civic Hospital Loeb Research Institute, Department of Medicine, University of Ottawa, Canada. | lld:pubmed |
| pubmed-article:9572482 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9572482 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9572482 | lld:pubmed |
