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Cell death: regulation by the Bcl‐2 protein family
Author(s) -
TSUJIMOTO Yoshihide
Publication year - 2006
Publication title -
psychogeriatrics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 32
eISSN - 1479-8301
pISSN - 1346-3500
DOI - 10.1111/j.1479-8301.2006.00173.x
Subject(s) - mitochondrial apoptosis induced channel , mitochondrial permeability transition pore , microbiology and biotechnology , cytochrome c , apoptosis , programmed cell death , mitochondrion , inner mitochondrial membrane , mitochondrial membrane transport protein , bacterial outer membrane , caspase , translocase of the inner membrane , biology , apoptosome , bcl 2 family , chemistry , biochemistry , escherichia coli , gene
An increase in mitochondrial membrane permeability is central to cell death including apoptosis and necrosis. During apoptosis, permeabilization of outer mitochondrial membrane leads to the release of several apoptogenic factors, such as cytochrome c and Smac/Diablo, into the cytoplasm that activate downstream death programs, including apoptotic proteases called caspases, although the detailed mechanism of outer mitochondrial membrane permeabilization remains elusive. Although the mitochondrial membrane permeability transition (MPT), resulting in Δψ loss, mitochondrial swelling and rupture of the outer membrane has initially been proposed as a general mechanism for apoptotic permeabilization of outer mitochondrial membrane, the recent studies with cyclophilin D‐deficient mice indicate that MPT regulates some forms of necrotic death, but not apoptotic death, and that MPT is involved in ischemia–reperfusion injury in heart and brain. Anti‐apoptotic proteins, Bcl‐2 and Bcl‐x L , efficiently block not only apoptotic mitochondrial permeabilization but also MPT. The present paper focuses on the mechanisms by which Bcl‐2 family members control the permeability of mitochondrial membrane during apoptosis and necrosis.