Journal
CELL DEATH AND DIFFERENTIATION
Volume 13, Issue 8, Pages 1387-1395Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401949
Keywords
MAC; mitochondrial apoptosis-induced channel; apoptosis; cytochrome c; patch-clamp; Bcl-2; Bax; t-Bid
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Funding
- NIGMS NIH HHS [GM57249] Funding Source: Medline
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Apoptosis is a phenomenon fundamental to higher eukaryotes and essential to mechanisms controlling tissue homeostasis. 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 proapoptotic factors. Mitochondrial apoptosis-induced channel (MAC) is the mitochondrial apoptosisinduced channel and is responsible for cytochrome c release early in apoptosis. MAC activity is detected by patch clamping mitochondria at the time of cytochrome c release. The Bcl-2 family proteins regulate apoptosis by controlling the formation of MAC. Depending on cell type and apoptotic inducer, Bax and/or Bak are structural component(s) of MAC. Overexpression of the antiapoptotic protein Bcl-2 eliminates MAC activity. The focus of this review is a biophysical characterization of MAC activity and its regulation by Bcl-2 family proteins, and ends with some discussion of therapeutic targets.
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