| pubmed-article:11046147 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0221908 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0206364 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0025646 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0085536 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0600388 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1335280 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1706044 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C0026559 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:11046147 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:11046147 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:11046147 | pubmed:dateCreated | 2000-12-19 | lld:pubmed |
| pubmed-article:11046147 | pubmed:abstractText | Epithelial morphogenesis is critical during development and wound healing, and alterations in this program contribute to neoplasia. Met, the hepatocyte growth factor (HGF) receptor, promotes a morphogenic program in epithelial cell lines in matrix cultures. Previous studies have identified Gab1, the major phosphorylated protein following Met activation, as important for the morphogenic response. Gab1 is a docking protein that couples the Met receptor with multiple signaling proteins, including phosphatidylinositol-3 kinase, phospholipase Cgamma, the adapter protein Crk, and the tyrosine specific phosphatase SHP-2. HGF induces sustained phosphorylation of Gab1 and sustained activation of extracellular signal-regulated kinase (Erk) in epithelial Madin-Darby canine kidney cells. In contrast, epidermal growth factor fails to promote a morphogenic program and induces transient Gab1 phosphorylation and Erk activation. To elucidate the Gab1-dependent signals required for epithelial morphogenesis, we undertook a structure-function approach and demonstrate that association of Gab1 with the tyrosine phosphatase SHP-2 is required for sustained Erk activation and for epithelial morphogenesis downstream from the Met receptor. Epithelial cells expressing a Gab1 mutant protein unable to recruit SHP-2 elicit a transient activation of Erk in response to HGF. Moreover, SHP-2 catalytic activity is required, since the expression of a catalytically inactive SHP-2 mutant, C/S, abrogates sustained activation of Erk and epithelial morphogenesis by the Met receptor. These data identify SHP-2 as a positive modulator of Erk activity and epithelial morphogenesis downstream from the Met receptor. | lld:pubmed |
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| pubmed-article:11046147 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11046147 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11046147 | pubmed:citationSubset | IM | lld:pubmed |
