The BCL-2 family proteins are key regulators of apoptosis and autophagy. The founding member BCL-2, which possesses four conserved BCL-2 homology domains (BH1–4), suppresses apoptosis through its interaction with and sequestration of pro-apoptotic proteins, such as Bax and Bak. Bax and Bak can oligomerize into proteolipid pores and permeabilize the outer mitochondrial membrane, resulting in the release of cytochrome c and other intermembrane factors into the cytosol to initiate downstream apoptotic events. The ratio between the anti-apoptotic and pro-apoptotic BCL-2 family members determines the sensitivity to apoptotic stimuli.
Anti-Human/Mouse BCL-2 (EPR17509)-146Nd—25 µg