| Literature DB >> 12853475 |
Catherine Yan1, Narcisa Martinez-Quiles, Sharon Eden, Tomoyuki Shibata, Fuminao Takeshima, Reiko Shinkura, Yuko Fujiwara, Roderick Bronson, Scott B Snapper, Marc W Kirschner, Raif Geha, Fred S Rosen, Frederick W Alt.
Abstract
The Wiskott-Aldrich syndrome related protein WAVE2 is implicated in the regulation of actin-cytoskeletal reorganization downstream of the small Rho GTPase, Rac. We inactivated the WAVE2 gene by gene-targeted mutation to examine its role in murine development and in actin assembly. WAVE2-deficient embryos survived until approximately embryonic day 12.5 and displayed growth retardation and certain morphological defects, including malformations of the ventricles in the developing brain. WAVE2-deficient embryonic stem cells displayed normal proliferation, whereas WAVE2-deficient embryonic fibroblasts exhibited severe growth defects, as well as defective cell motility in response to PDGF, lamellipodium formation and Rac-mediated actin polymerization. These results imply a non-redundant role for WAVE2 in murine embryogenesis and a critical role for WAVE2 in actin-based processes downstream of Rac that are essential for cell movement.Entities:
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Year: 2003 PMID： 12853475 PMCID： PMC165620 DOI： 10.1093/emboj/cdg350
Source DB: PubMed Journal: EMBO J ISSN： 0261-4189 Impact factor: 11.598