Evidence That β3 Integrin-Induced Rac Activation Involves the Calpain-Dependent Formation of Integrin Clusters That Are Distinct from the Focal Complexes and Focal Adhesions That Form as Rac and Rhoa Become Active
| Autor: | Xiaoping Du, Katarzyna Bialkowska, Sucheta Kulkarni, Joan E.B. Fox, Takaomi C. Saido, Darrel E. Goll |
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| Jazyk: | angličtina |
| Rok vydání: | 2000 |
| Předmět: |
β3 integrin
RHOA Macromolecular Substances Integrin Platelet Membrane Glycoproteins Models Biological Focal adhesion cell spreading integrin clusters Antigens CD Cell Adhesion Animals Humans Vitronectin Cell adhesion Cytoskeleton Aorta Cells Cultured Cell Size Genes Dominant Focal Adhesions biology Calpain Integrin beta3 Cell Biology Vinculin Cell biology Fibronectins rac GTP-Binding Proteins Rac GTP-Binding Proteins Enzyme Activation Amino Acid Substitution Mutation biology.protein Original Article Cattle Cell Surface Extensions Endothelium Vascular rhoA GTP-Binding Protein Protein Processing Post-Translational Rac activation Protein Binding Signal Transduction |
| Zdroj: | The Journal of Cell Biology |
| ISSN: | 1540-8140 0021-9525 |
| Popis: | Interaction of integrins with the extracellular matrix leads to transmission of signals, cytoskeletal reorganizations, and changes in cell behavior. While many signaling molecules are known to be activated within Rac-induced focal complexes or Rho-induced focal adhesions, the way in which integrin-mediated adhesion leads to activation of Rac and Rho is not known. In the present study, we identified clusters of integrin that formed upstream of Rac activation. These clusters contained a Rac-binding protein(s) and appeared to be involved in Rac activation. The integrin clusters contained calpain and calpain-cleaved β3 integrin, while the focal complexes and focal adhesions that formed once Rac and Rho were activated did not. Moreover, the integrin clusters were dependent on calpain for their formation. In contrast, while Rac- and Rho-GTPases were dependent on calpain for their activation, formation of focal complexes and focal adhesions by constitutively active Rac or Rho, respectively, occurred even when calpain inhibitors were present. Taken together, these data are consistent with a model in which integrin-induced Rac activation requires the formation of integrin clusters. The clusters form in a calpain-dependent manner, contain calpain, calpain-cleaved integrin, and a Rac binding protein(s). Once Rac is activated, other integrin signaling complexes are formed by a calpain-independent mechanism(s). |
| Databáze: | OpenAIRE |
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