Baff regulates B cell survival by downregulating the BH3-only homolog Bim via the ERK pathway

CRAXTON A,; DRAVES K; GRUPPI A; CLARK EA

Rockefeller University Press.

Lugar: New York (USA); Año: 2005 p. 1363 - 1363

table id="HB_Mail_Container" height="100%" cellspacing="0" cellpadding="0" width="100%" border="0" unselectable="on"> The B cell activating factor belonging to the tumor necrosis factor family (BAFF) is required for B cell survival and maturation. The mechanisms by which BAFF mediates B cell survival are less understood. We found that BAFF and a proliferation-inducing ligand (APRIL), which are related, block B cell antigen receptor (BCR)-induced apoptosis upstream of mitochondrial damage, which is consistent with a role for Bcl-2 family proteins. BCR ligation strongly increased expression of the proapoptotic Bcl-2 homology 3-only Bcl-2 protein Bim in both WEHI-231 and splenic B cells, and increases in Bim were reversed by BAFF or APRIL. Small interfering RNA vector-mediated suppression of Bim blocked BCR-induced apoptosis. BAFF