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PubMed · 15941910

Vav proteins regulate peripheral B-cell survival.

Elena Vigorito·Laure Gambardella·Francesco Colucci·Simon McAdam·Martin Turner
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Abstract

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.

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AnimalsApoptosisB-LymphocytesBlotting, WesternBone Marrow CellsBromodeoxyuridineCell NucleusCell ProliferationCell SeparationCell SurvivalColoring AgentsCross-Linking ReagentsDown-RegulationFlow CytometryGene Expression RegulationGuanine Nucleotide Exchange FactorsMiceMutationNF-kappa BProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-relProto-Oncogene Proteins c-vavReceptors, Antigen, B-CellRecombinant Fusion ProteinsSignal TransductionSpleenTime FactorsTranscription Factor RelATransgenesJournal ArticleResearch Support, Non-U.S. Gov't

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Elena Vigorito, Laure Gambardella, Francesco Colucci, Simon McAdam, Martin Turner. 2005-06-07. Vav proteins regulate peripheral B-cell survival.. https://doi.org/10.1182/blood-2004-12-4894

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