Selective regulation of integrin--cytoskeleton interactions by the tyrosine kinase Src.

摘要: Cell motility on extracellular-matrix (ECM) substrates depends the regulated generation of force against substrate through adhesion receptors known as integrins. Here we show that integrin-mediated traction forces can be selectively modulated by tyrosine kinase Src. In Src-deficient fibroblasts, cell spreading ECM component vitronectin is inhibited, while strengthening linkages between integrin and force-generating cytoskeleton in response to rigidity dramatically increased. contrast, Src deficiency has no detectable effects fibronectin-receptor function. Finally, truncated (lacking domain) co-localizes focal-adhesion sites with αv but not β1 These data are consistent a selective, functional interaction receptor acts at integrin–cytoskeleton interface regulate migration.