Protein kinase A‐dependent increase in WAVE2 expression induced by the focal adhesion protein vinexin
Copyright policy )Protein kinase A‐dependent increase in WAVE2 expression induced by the focal adhesion protein vinexin
The focal adhesion protein vinexin is a member of a family of adaptor proteins that are thought to participate in the regulation of cell adhesion, cytoskeletal reorganization, and growth factor signaling. Here, we show that vinexin β increases the amount of and reduces the mobility on SDS‐PAGE of Wiskott‐Aldrich syndrome protein family verprolin‐homologous protein (WAVE) 2 protein, which is a key factor modulating actin polymerization in migrating cells. This mobility retardation disappeared after in vitro phosphatase treatment. Co‐immunoprecipitation assays revealed the interaction of vinexin β with WAVE2 as well as WAVE1 and N‐WASP. Vinexin β interacts with the proline‐rich region of WAVE2 through the first and second SH3 domains of vinexin β. Mutations disrupting the interaction impaired the ability of vinexin β to increase the amount of WAVE2 protein. Treatments with proteasome inhibitors increased the amount of WAVE2, but did not have an additive effect with vinexin β. Inhibition of protein kinase A (PKA) activity suppressed the vinexin‐induced increase in WAVE2 protein, while activation of PKA increased WAVE2 expression without vinexin β. These results suggest that vinexin β regulates the proteasome‐dependent degradation of WAVE2 in a PKA‐dependent manner.
- Kyoto University Japan
- University of Tokyo Japan
Focal Adhesions, Muscle Proteins, Wiskott-Aldrich Syndrome Protein, Neuronal, Cyclic AMP-Dependent Protein Kinases, Actins, Wiskott-Aldrich Syndrome Protein Family, Enzyme Activation, src Homology Domains, Mice, Cell Movement, Mutation, NIH 3T3 Cells, Phosphoprotein Phosphatases, Animals, Immunoprecipitation, Electrophoresis, Polyacrylamide Gel, Protease Inhibitors, Proteasome Inhibitors, Protein Binding
Focal Adhesions, Muscle Proteins, Wiskott-Aldrich Syndrome Protein, Neuronal, Cyclic AMP-Dependent Protein Kinases, Actins, Wiskott-Aldrich Syndrome Protein Family, Enzyme Activation, src Homology Domains, Mice, Cell Movement, Mutation, NIH 3T3 Cells, Phosphoprotein Phosphatases, Animals, Immunoprecipitation, Electrophoresis, Polyacrylamide Gel, Protease Inhibitors, Proteasome Inhibitors, Protein Binding
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