Key result
Loss of Cav1 induces an increase in Rac1 protein and its activated form by regulating ubiquitylation and degradation of activated Rac1 in an adhesion-dependent fashion.
Population
Cav1-deficient mouse fibroblasts and human epithelial and endothelial cells
Design
Preclinical
Authors
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No immediate clinical implications; leaves open Cav1-Rac1 targeting for future cardiovascular migration studies.
This study uncovers Cav1-regulated polyubiquitylation as a novel mechanism controlling Rac1 signaling and degradation during cell migration.
Nethe et al. (2010) studied this question. Depletion of Cav1 expression vs. Normal Cav1 expression was evaluated on Rac1 protein levels and activation. Loss of Cav1 induces an increase in Rac1 protein and its activated form by regulating ubiquitylation and degradation of activated Rac1 in an adhesion-dependent fashion.