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Nat Immunol. 2001 Jun;2(6):548-55.

Compensation between Vav-1 and Vav-2 in B cell development and antigen receptor signaling.

Author information

1
Abteilung Physiologische Chemie, Universit├Ąt Ulm, Albert-Einstein-Allee 11, D-89069 Ulm, Germany.

Abstract

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.

Comment in

PMID:
11376343
DOI:
10.1038/88756
[Indexed for MEDLINE]

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