Function
BCL-2 (B-cell lymphoma 2) is an important regulator of apoptosis, a process of programmed cell death. It suppresses apoptosis in a variety of cell systems, including factor-dependent lymphohematopoietic and neural cells. BCL-2 regulates cell death by controlling mitochondrial membrane permeability, acting as a critical checkpoint in the apoptotic cascade. It appears to function in a feedback loop system with caspases, a family of proteases involved in apoptosis. BCL-2 inhibits caspase activity by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). It also acts as an inhibitor of autophagy, a process of cellular self-digestion. BCL-2 interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function. Additionally, BCL-2 may attenuate inflammation by impairing NLRP1-inflammasome activation, thus inhibiting CASP1 activation and IL1B release.