Focal adhesion kinase modulates cell adhesion strengthening via integrin activation.

Michael KE, Dumbauld DW, Burns KL, Hanks SK, GarcĂ­a AJ
Mol Biol Cell. 2009 20 (9): 2508-19

PMID: 19297531 · PMCID: PMC2675629 · DOI:10.1091/mbc.e08-01-0076

Focal adhesion kinase (FAK) is an essential nonreceptor tyrosine kinase regulating cell migration, adhesive signaling, and mechanosensing. Using FAK-null cells expressing FAK under an inducible promoter, we demonstrate that FAK regulates the time-dependent generation of adhesive forces. During the early stages of adhesion, FAK expression in FAK-null cells enhances integrin activation to promote integrin binding and, hence, the adhesion strengthening rate. Importantly, FAK expression regulated integrin activation, and talin was required for the FAK-dependent effects. A role for FAK in integrin activation was confirmed in human fibroblasts with knocked-down FAK expression. The FAK autophosphorylation Y397 site was required for the enhancements in adhesion strengthening and integrin-binding responses. This work demonstrates a novel role for FAK in integrin activation and the time-dependent generation of cell-ECM forces.

MeSH Terms (19)

Animals Biomechanical Phenomena Cell Adhesion Fibroblasts Fibronectins Focal Adhesion Protein-Tyrosine Kinases Gene Knockdown Techniques Humans Integrin alpha5beta1 Integrins Kinetics Mice Phosphorylation Phosphotyrosine Protein Binding Solubility Talin Tetracycline Vinculin

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