| http://purl.uniprot.org/citations/12529399 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12529399 | http://www.w3.org/2000/01/rdf-schema#comment | "R-Ras regulates integrin function, but its effects on integrin signaling pathways have not been well described. We demonstrate that activation of R-Ras promoted focal adhesion formation and altered localization of the alpha2beta1 integrin from cell-cell to cell-matrix adhesions in breast epithelial cells. Constitutively activated R-Ras(38V) dramatically enhanced focal adhesion kinase (FAK) and p130(Cas) phosphorylation upon collagen stimulation or clustering of the alpha2beta1 integrin, even in the absence of increased ligand binding. Signaling events downstream of R-Ras differed from integrins and K-Ras, since pharmacological inhibition of Src or disruption of actin inhibited integrin-mediated FAK and p130(Cas) phosphorylation, focal adhesion formation, and migration in control and K-Ras(12V)-expressing cells but had minimal effect in cells expressing R-Ras(38V). Therefore, signaling from R-Ras to FAK and p130(Cas) has a component that is Src independent and not through classic integrin signaling pathways and a component that is Src dependent. R-Ras effector domain mutants and pharmacological inhibition suggest a partial role for phosphatidylinositol 3-kinase (PI3K), but not Raf, in R-Ras signaling to FAK and p130(Cas). However, PI3K cannot account for the Src-independent pathway, since simultaneous inhibition of both PI3K and Src did not completely block effects of R-Ras on FAK phosphorylation. Our results suggest that R-Ras promotes focal adhesion formation by signaling to FAK and p130(Cas) through a novel mechanism that differs from but synergizes with the alpha2beta1 integrin."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.23.3.933-949.2003"xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/author | "Keely P.J."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/author | "Wilson S.D."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/author | "Wozniak M.A."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/author | "Kwong L."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/author | "Collins A.S."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/name | "Mol Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/pages | "933-949"xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/title | "R-Ras promotes focal adhesion formation through focal adhesion kinase and p130(Cas) by a novel mechanism that differs from integrins."xsd:string |
| http://purl.uniprot.org/citations/12529399 | http://purl.uniprot.org/core/volume | "23"xsd:string |
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