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      Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.

      Science (New York, N.Y.)

      Apoproteins, metabolism, Apoptosis, Caspase 3, Caspases, Cysteine Endopeptidases, Cytochrome c Group, Cytochromes c, Cytosol, DNA Fragmentation, Enzyme Activation, Etoposide, pharmacology, HL-60 Cells, HeLa Cells, Humans, Intracellular Membranes, Membrane Potentials, drug effects, Mitochondria, Poly(ADP-ribose) Polymerases, Proto-Oncogene Proteins c-bcl-2, genetics, Staurosporine, Transfection

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          Abstract

          Bcl-2 is an integral membrane protein located mainly on the outer membrane of mitochondria. Overexpression of Bcl-2 prevents cells from undergoing apoptosis in response to a variety of stimuli. Cytosolic cytochrome c is necessary for the initiation of the apoptotic program, suggesting a possible connection between Bcl-2 and cytochrome c, which is normally located in the mitochondrial intermembrane space. Cells undergoing apoptosis were found to have an elevation of cytochrome c in the cytosol and a corresponding decrease in the mitochondria. Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria.

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          9027314

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