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Mice lacking all 3 Vav proteins fail to produce significant numbers of recirculating follicular or marginal zone B cells. Those B cells that do mature have shortened lifespans. The constitutive nuclear factor-kappaB (NF-kappaB) activity of resting naive B cells required Vav function and expression of cellular reticuloendotheliosis (c-Rel). Rel-A was reduced in Vav-deficient B cells. Furthermore, expression of the NF-kappaB-regulated antiapoptotic genes A1 and Bcl-2 was reduced in mature Vav-deficient B cells. Overexpression of Bcl-2 restored the number of mature follicular B cells in the spleens of Vav-deficient mice. When activated by B-cell receptor (BCR) cross-linking, Vav-deficient B cells failed to activate NF-kappaB. Vav proteins thus regulate an NF-kappaB-dependent survival signal in naive B cells and are required for NF-kappaB function after BCR cross-linking.

Original publication




Journal article



Publication Date





2391 - 2398


Animals, Apoptosis, B-Lymphocytes, Blotting, Western, Bone Marrow Cells, Bromodeoxyuridine, Cell Nucleus, Cell Proliferation, Cell Separation, Cell Survival, Coloring Agents, Cross-Linking Reagents, Down-Regulation, Flow Cytometry, Gene Expression Regulation, Guanine Nucleotide Exchange Factors, Mice, Mutation, NF-kappa B, Proto-Oncogene Proteins c-bcl-2, Proto-Oncogene Proteins c-rel, Proto-Oncogene Proteins c-vav, Receptors, Antigen, B-Cell, Recombinant Fusion Proteins, Signal Transduction, Spleen, Time Factors, Transcription Factor RelA, Transgenes