## Abstract Although it has been long recognized that the relative balance of pro‐ and antiapoptotic Bcl‐2 proteins is critical in determining the susceptibility to apoptotic death, only a few studies have examined the level of these proteins specifically at mitochondria during postnatal brain deve
Cell death regulation by the Bcl-2 protein family in the mitochondria
✍ Scribed by Yoshihide Tsujimoto
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 271 KB
- Volume
- 195
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
An increase in the permeability of the outer mitochondrial membrane is central to apoptotic cell death, since it leads to the release of several apoptogenic factors, such as cytochrome c and Smac/Diablo, into the cytoplasm that activate downstream death programs. During apoptosis, the mitochondria also release AIF and endonuclease G, both of which are translocated to the nucleus and are implicated in apoptotic nuclear changes that occur in a caspase‐independent manner. Mitochondrial membrane permeability is directly controlled by the major apoptosis regulator, i.e., the Bcl‐2 family of proteins, mainly through regulation of the formation of apoptotic protein‐conducting pores in the outer mitochondrial membrane, although the precise molecular mechanisms are still not completely understood. Here, I focus on the mechanisms by which Bcl‐2 family members control the permeability of mitochondrial membrane during apoptosis. © 2003 Wiley‐Liss, Inc.
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