" /> Extracellular Matrix Binding Pathway - CISMeF





Preferred Label : Extracellular Matrix Binding Pathway;

NCIt related terms : Erk and PI-3 Kinase Are Necessary for Collagen Binding in Corneal Epithelia;

Alternative definition : BIOCARTA: Activation of the MAPK kinase pathway has been identified as a mechanism that integrins use to regulate gene expression, leading to cell shape changes during cell spreading or migration. Epithelial cells respond to extracellular matrix (ECM) causing integrin-mediated FAK phosphorylation; this, in turn, phosphorylates the surrounding proteins (paxillin, Fyn/shc, and src) and leads to signal amplification. FAK also binds PI-3 kinase and acts upstream in the MAP kinase pathway. When MAP kinase or PI-3 kinase is inhibited, actin reorganization is blocked. Src phosphorylates p190RhoGAP, inactivating its GAP function and allowing RhoGTP to stay active longer, promoting further signal amplification. Activated RhoGTP binds to downstream kinases such as Rho-associated coiled coil-containing protein kinase (p160ROCK) and p140 diaphanous (p140Dia) to increase actin polymerization and contraction. Actin reorganization assists integrin clustering, allowing more ECM binding that increase FAK phosphorylation and other signal transduction events. (This definition may be outdated - see the DesignNote.);

NCIt note : The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA Definition might be outdated or inaccurate. Please see the Terms and Conditions for Use at http://www.biocarta.com/.;

Biocarta ID : h_ecmPathway;

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14/05/2024


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