Actin cytoskeletal function is spared, but apoptosis is increased, in WAS patient hematopoietic cells

Abstract excerpt

Mutations in the Wiskott-Aldrich syndrome protein (WASP) have been hypothesized to cause defective actin cytoskeletal function. This resultant dysfunction of the actin cytoskeleton has been implicated in the pathogenesis of Wiskott-Aldrich syndrome (WAS). In contrast, it was found that stimulated actin polymerization is kinetically normal in the hematopoietic lineages affected in WAS. It was also found that the...

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Cell Adhesion Molecules Research
• Share to Cellular Mechanics and Interactions
• Share to Protein Kinase Regulation and GTPase Signaling