![]() ![]() In mammals, there are five members: BCL-2 itself, BCL-XL, BCL-W, MCL-1 and BFL-1. The last faction within the BCL-2 family are the “BCL-2-like” pro-survival proteins. A consequence of this event is the release of apoptogenic factors such as cytochrome c from the mitochondria into the cytosol, leading to activation of the cellular demolitionists, the caspases. These multi-domain proteins, once activated, oligomerise to form pores resulting in mitochondrial outer membrane permeabilisation. This family which includes BAX, BAK and BOK are the downstream effectors of the family. ![]() The second sub-family of death-promoting molecules are the “BAX/BAK-like” proteins. In mammals, there are eight main members including BIM, PUMA, BID, NOXA, BID, BAD, BMF and HRK. ![]() Upon receipt of a death stimulus, these BH3-only proteins are transcriptionally upregulated, or post-translationally modified, enabling them to act on downstream pro- and anti-apoptotic family members, thereby initiating the slippery slide to cell death. The first comprise the “BH3-only” proteins which trigger the apoptotic cascade. Of the cell death promoters, there are two sub-families. Within the BCL-2 family, there are proteins that promote cell death and others that enable cell survival. These events lead to BAX/BAK oligomerization followed by mitochondrial outer membrane permeabilisation, caspase activation and death. The BH3-only proteins trigger the apoptotic cascade by either binding the BCL-2-like pro-survival proteins, displacing the BAX/BAK-like proteins, or alternatively in the case of certain members (e.g., BIM, BID, PUMA), by directly engaging and activating BAX/BAK. ![]()
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