| pubmed-article:10744748 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10744748 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:10744748 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:10744748 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:10744748 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:10744748 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:10744748 | pubmed:dateCreated | 2000-5-8 | lld:pubmed |
| pubmed-article:10744748 | pubmed:abstractText | The insulin receptor substrate (IRS) family of proteins mediate a variety of intracellular signaling events by serving as signaling platforms downstream of several receptor tyrosine kinases including the insulin and insulin-like growth factor-1 (IGF-1) receptors. Recently, several new members of this family have been identified including IRS-3, IRS-4, and growth factor receptor-binding protein 2-associated binder-1 (Gab-1). 3T3 cell lines derived from IRS-1-deficient embryos exhibit a 70-80% reduction in IGF-1-stimulated S-phase entry and a parallel decrease in the induction of the immediate-early genes c-fos and egr-1 but unaltered activation of the mitogen-activated protein kinases extracellular signal-regulated kinase-1 and extracellular signal-regulated kinase-2. Reconstitution of IRS-1 expression in IRS-1-deficient fibroblasts by retroviral mediated gene transduction is capable of restoring these defects. Overexpression of Gab-1 in IRS-1-deficient fibroblasts also results in the restoration of egr-1 induction to levels similar to those achieved by IRS-1 reconstitution and markedly increases IGF-1-stimulated S-phase progression. Gab-1 is capable of regulating these biological end points despite the absence of IGF-1 stimulated tyrosine phosphorylation. These data provide evidence that Gab-1 may serve as a unique signaling intermediate in insulin/IGF-1 signaling for induction of early gene expression and stimulation of mitogenesis without direct tyrosine phosphorylation. | lld:pubmed |
| pubmed-article:10744748 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10744748 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10744748 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10744748 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10744748 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10744748 | pubmed:author | pubmed-author:KahnC RCR | lld:pubmed |
| pubmed-article:10744748 | pubmed:author | pubmed-author:BurksD JDJ | lld:pubmed |
| pubmed-article:10744748 | pubmed:author | pubmed-author:BrüningJ CJC | lld:pubmed |
| pubmed-article:10744748 | pubmed:author | pubmed-author:WinnayJ NJN | lld:pubmed |
| pubmed-article:10744748 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10744748 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:10744748 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:10744748 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10744748 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10744748 | pubmed:pagination | 10545-50 | lld:pubmed |
| pubmed-article:10744748 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:meshHeading | pubmed-meshheading:10744748... | lld:pubmed |
| pubmed-article:10744748 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10744748 | pubmed:articleTitle | Gab-1-mediated IGF-1 signaling in IRS-1-deficient 3T3 fibroblasts. | lld:pubmed |
| pubmed-article:10744748 | pubmed:affiliation | Division of Cellular and Molecular Physiology, Joslin Diabetes Center and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA. | lld:pubmed |
| pubmed-article:10744748 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10744748 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10744748 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10744748 | lld:pubmed |
