Abstract

Mitochondria-mediated apoptosis involves efflux of a number of potential apoptotic regulators, such as cytochrome c, to the cytosol, triggering the caspase cascade and cell destruction. The precise mechanism regulating cytochrome c release remains unknown, and the molecular architecture of the cytochrome c-conducting channel has also to be determined. There is substantial evidence suggesting that the voltage-dependent anion channel-1 (VDAC1) is a critical player in apoptosis by regulating the release of apoptogenic proteins from mitochondria in mammalian cells and interacting with pro- and anti-apoptotic proteins.

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