Life-or-death decisions by the Bcl-2 protein family.

By Jerry M. Adams, Suzanne Cory. TIBS -Trends in Biochemical Sciences. Regular ed, 2001

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Mechanisms of ischemic brain damage. (2008, neutral): “Unlike Bax and Bak, Bid, Bad and Bim do not have the ability to directly mediate cytochrome c release by forming a pore.”
The role of mitochondria in apoptosis. (2008, background): “The pro-apoptotic members can be divided into two groups (22, 23): those with BH1, BH2 and BH3 domains, such as Bax and Bak, and”
Coupling endoplasmic reticulum stress to the cell death program (2004, background): “, Bad, Bid, Bim, Bik).(112,113) On activation, the proapoptotic Bax and Bak”
Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis (2015, background): “Bcl-2 family proteins can be readily heterodimerized by protein-protein interactions between pro- and anti-apoptotic Bcl-2 family members, which determine whether cell survival or the apoptosis signal proceed [25,26].”
OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, positive): “Proteins of the BCL-2 family control the release of cytochrome c from mitochondria required for the activation of effector caspases (Adams and Cory, 2001).”