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Blood, 1 October 2005, Vol. 106, No. 7, pp. 2391-2398. Prepublished online as a Blood First Edition Paper on June 7, 2005; DOI 10.1182/blood-2004-12-4894. This Article Full Text (PDF) All Versions of this Article: 2004-12-4894v1 106/7/2391    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Vigorito, E. Articles by Turner, M. Search for Related Content PubMed PubMed Citation Articles by Vigorito, E. Articles by Turner, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 23, 2004 Accepted May 26, 2005 Vav proteins regulate peripheral B cell survival Elena Vigorito*, Laure Gambardella, Francesco Colucci, Simon McAdam, and Martin Turner Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Cambridge, United Kingdom * Corresponding author; email: elena.vigorito{at}bbsrc.ac.uk. Mice lacking all three Vav proteins fail to produce significant numbers of recirculating follicular or marginal zone B cells. Those B cells that do mature have a shortened lifespan. The constitutive NF-B activity of resting naive B cells required Vav function and expression of c-Rel, Rel-A was reduced in Vav deficient B cells. Furthermore, the expression of the NF-B regulated anti-apoptotic genes A1 and Bcl-2 was reduced in mature Vav-deficient B cells. Over-expression of Bcl-2 restored the number of mature follicular B cells in the spleen of Vav deficient mice. When activated by BCR crosslinking Vav deficient B cells failed to activate NF-B. The Vav proteins thus regulate a NF-B dependent survival signal in naive B cells and are required for NF-B function following BCR crosslinking. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Castro, J. A. Wright, B. Damdinsuren, K. L. Hoek, G. Carlesso, N. P. Shinners, R. M. Gerstein, R. T. Woodland, R. Sen, and W. N. Khan B Cell Receptor-Mediated Sustained c-Rel Activation Facilitates Late Transitional B Cell Survival through Control of B Cell Activating Factor Receptor and NF-{kappa}B2 J. Immunol., June 15, 2009; 182(12): 7729 - 7737. [Abstract] [Full Text] [PDF] C. Dumont, A. Corsoni-Tadrzak, S. Ruf, J. de Boer, A. Williams, M. Turner, D. Kioussis, and V. L. J. Tybulewicz Rac GTPases play critical roles in early T-cell development Blood, April 23, 2009; 113(17): 3990 - 3998. [Abstract] [Full Text] [PDF] A. D. Joshi, G. V. Hegde, J. D. Dickinson, A. K. Mittal, J. C. Lynch, J. D. Eudy, J. O. Armitage, P. J. Bierman, R. G. Bociek, M. P. Devetten, et al. ATM, CTLA4, MNDA, and HEM1 in High versus Low CD38 Expressing B-Cell Chronic Lymphocytic Leukemia Clin. Cancer Res., September 15, 2007; 13(18): 5295 - 5304. [Abstract] [Full Text] [PDF]

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