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 (This definition may be outdated - see the DesignNote.);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Definition might be outdated or inaccurate.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;
Origin ID : C39054;
UMLS CUI : C1517051;
Semantic type(s)
has_gene_product_element
pathway_has_gene_element