Compensation between Vav-1 and Vav-2 in B cell development and antigen receptor signaling
Compensation between Vav-1 and Vav-2 in B cell development and antigen receptor signaling
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DOI：
10.1038/88756
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发表时间：
2001-06-01
影响因子：
30.5
通讯作者：
Fischer, KD
中科院分区：
文献类型：
--
作者：
Tedford, K;Nitschke, L;Fischer, KD
Vav-1 and Vav-2 are closely related Dbl-homology CTP 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 Vav1(-/-)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.
