| First Author | Yan C | Year | 2003 |
| Journal | EMBO J | Volume | 22 |
| Issue | 14 | Pages | 3602-12 |
| PubMed ID | 12853475 | Mgi Jnum | J:84642 |
| Mgi Id | MGI:2668778 | Doi | 10.1093/emboj/cdg350 |
| Citation | Yan C, et al. (2003) WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility. EMBO J 22(14):3602-12 |
| abstractText | 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. |
