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Vav proteins regulate peripheral B-cell survival.

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.

journal_name

Blood

journal_title

Blood

authors

Vigorito E,Gambardella L,Colucci F,McAdam S,Turner M

doi

10.1182/blood-2004-12-4894

subject

Has Abstract

pub_date

2005-10-01 00:00:00

pages

2391-8

issue

7

eissn

0006-4971

issn

1528-0020

pii

2004-12-4894

journal_volume

106

pub_type

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