| First Author | Tedford K | Year | 2001 |
| Journal | Nat Immunol | Volume | 2 |
| Issue | 6 | Pages | 548-55 |
| PubMed ID | 11376343 | Mgi Jnum | J:69806 |
| Mgi Id | MGI:2135486 | Doi | 10.1038/88756 |
| Citation | Tedford K, et al. (2001) Compensation between Vav-1 and Vav-2 in B cell development and antigen receptor signaling. Nat Immunol 2(6):548-55 |
| abstractText | Vav-1 and Vav-2 are closely related Dbl-homology GTP exchange factors (GEFs) for Rho GTPases. Mutation of Vav-1 disrupts T cell development and T cell antigen receptor-induced activation, but has comparatively little effect on B cells. We found that combined deletion of both Vav-1 and Vav-2 in mice resulted in a marked reduction in mature B lymphocyte numbers. Vav-1(-/-)Vav-2(-/-) B cells were unresponsive to B cell antigen receptor (BCR)-driven proliferation in vitro and to thymus-independent antigen in vivo. BCR-stimulated intracellular calcium mobilization was greatly impaired in Vav-1(-/-)Vav-2(-/-) B cells. These findings establish a role for Vav-2 in BCR calcium signaling and reveal that the Vav family of GEFs is critical to B cell development and function. |
