The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
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- Ruth M. Kluck
- Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Park Drive, San Diego, CA 92121, USA.
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- Ella Bossy-Wetzel
- Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Park Drive, San Diego, CA 92121, USA.
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- Douglas R. Green
- Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Park Drive, San Diego, CA 92121, USA.
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- Donald D. Newmeyer
- Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Park Drive, San Diego, CA 92121, USA.
抄録
<jats:p>In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology. Bcl-2 acted in situ on mitochondria to prevent the release of cytochrome c and thus caspase activation. During apoptosis in intact cells, cytochrome c translocation was similarly blocked by Bcl-2 but not by a caspase inhibitor, zVAD-fmk. In vitro, exogenous cytochrome c bypassed the inhibitory effect of Bcl-2. Cytochrome c release was unaccompanied by changes in mitochondrial membrane potential. Thus, Bcl-2 acts to inhibit cytochrome c translocation, thereby blocking caspase activation and the apoptotic process.</jats:p>
収録刊行物
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- Science
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Science 275 (5303), 1132-1136, 1997-02-21
American Association for the Advancement of Science (AAAS)
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詳細情報
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- CRID
- 1363388844404158080
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- NII論文ID
- 80009498123
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- ISSN
- 10959203
- 00368075
- http://id.crossref.org/issn/00368075
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