| First Author | Vigorito E | Year | 2005 |
| Journal | Blood | Volume | 106 |
| Issue | 7 | Pages | 2391-8 |
| PubMed ID | 15941910 | Mgi Jnum | J:119378 |
| Mgi Id | MGI:3701919 | Doi | 10.1182/blood-2004-12-4894 |
| Citation | Vigorito E, et al. (2005) Vav proteins regulate peripheral B-cell survival. Blood 106(7):2391-8 |
| abstractText | 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. |
