Abstract
The commitment to programmed cell death involves complex interactions among pro- and antiapoptotic members of the Bcl-2 family of proteins. The physiological result of a decision by these proteins to undergo cell death is permeabilization of the mitochondrial outer membrane. Pharmacologic manipulation of proteins in this family appears both feasible and efficacious, whether the goal is decreased cell death, as in ischemia of the myocardium or brain, or increased cell death, as in cancer.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Brain Ischemia / drug therapy
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Brain Ischemia / metabolism*
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Cell Death / physiology
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Cell Membrane Permeability / drug effects
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Drug Delivery Systems / methods
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Drug Design
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Humans
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Mitochondria / drug effects
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Mitochondria / metabolism*
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Myocardial Ischemia / drug therapy
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Myocardial Ischemia / metabolism*
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Neoplasms / drug therapy
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Neoplasms / metabolism*
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Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
Substances
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Proto-Oncogene Proteins c-bcl-2