Cell death regulation by the Bcl-2 protein family in the mitochondria

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 a...

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Bibliographic Details
Published in:Journal of cellular physiology 2003-05, Vol.195 (2), p.158-167
Main Author: Tsujimoto, Yoshihide
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Cell Membrane Permeability - physiology
Eukaryotic Cells - metabolism
Humans
Intracellular Membranes - metabolism
Mitochondria - metabolism
Protein Structure, Tertiary - physiology
Protein Transport - physiology
Proto-Oncogene Proteins c-bcl-2 - genetics
Proto-Oncogene Proteins c-bcl-2 - metabolism
Signal Transduction - physiology
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Summary: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.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.10254