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BAX is a pro-apoptotic member of the Bcl-2 protein family that plays a critical role in initiating apoptosis. Upon activation by cellular stress signals, BAX translocates to the mitochondria, oligomerizes, and permeabilizes the outer mitochondrial membrane, leading to the release of cytochrome c and other pro-apoptotic factors. This initiates the caspase cascade and ultimately results in programmed cell death. Dysregulation of BAX is implicated in various cancers, making it an important therapeutic target for restoring apoptotic sensitivity in cancer cells.
Drugs aim to restore BAX-mediated apoptosis in cancer cells by promoting its activation, translocation to mitochondria, and oligomerization, leading to cytochrome c release and caspase activation.
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