Mitochondria-Dependent Caspase-9 Activation Is Necessary for Antigen Receptor-Mediated Effector Caspase Activation and Apoptosis in WEHI 231 Lymphoma Cells

摘要: Engagement of the B cell Ag receptor (BCR) on immature cells leads to growth arrest followed by apoptosis. Concomitant signaling through CD40 sustains proliferation and rescues from Previously, we have shown that cross-linking stimulates expression A1, an antiapoptotic member Bcl-2 family, transduction murine lymphoma line WEHI 231, a model for cells, with A1 protected against BCR-induced Here demonstrate strongly interferes activation caspase-7, major effector caspase activated after BCR 231 cells. The pathway leading cascade including caspase-7 is unclear. Using retrovirally transduced populations, show catalytically inactive mutant cleaved almost as efficiently wild-type form, arguing autocatalysis sole activating process. In contrast, overexpression caspase-9 processing, poly(ADP-ribose) polymerase cleavage, DNA laddering, suggesting role hence mitochondrial pathway. importance mitochondrial/caspase-9 BCR-triggered apoptosis highlighted our finding both attenuate Thus, data suggest BCR-mediated apoptotic signal in spreads via