Literature DB >> 16055309

Regulation of the mitochondrial apoptosis-induced channel, MAC, by BCL-2 family proteins.

Laurent M Dejean1, Sonia Martinez-Caballero, Stephen Manon, Kathleen W Kinnally.   

Abstract

Programmed cell death or apoptosis is central to many physiological processes and pathological conditions such as organogenesis, tissue homeostasis, cancer, and neurodegenerative diseases. Bcl-2 family proteins tightly control this cell death program by regulating the permeabilization of the mitochondrial outer membrane and, hence, the release of cytochrome c and other pro-apoptotic factors. Control of the formation of the mitochondrial apoptosis-induced channel, or MAC, is central to the regulation of apoptosis by Bcl-2 family proteins. MAC is detected early in apoptosis by patch clamping the mitochondrial outer membrane. The focus of this review is on the regulation of MAC activity by Bcl-2 family proteins. The role of MAC as the putative cytochrome c release channel during early apoptosis and insights concerning its molecular composition are also discussed.

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Year:  2005        PMID: 16055309     DOI: 10.1016/j.bbadis.2005.07.002

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  60 in total

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Review 3.  The role of the mitochondrial apoptosis induced channel MAC in cytochrome c release.

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9.  Long non-coding RNA ZEB2-AS1 promotes proliferation and inhibits apoptosis in human lung cancer cells.

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