Pharmacological manipulation of Bcl-2 family members to control cell death.
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.
Letai
Anthony
A
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. anthony_letai@dfci.harvard.edu
D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism*; D016923:Cell Death / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects; D016503:Drug Delivery Systems / Q000379:methods; D015195:Drug Design; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000378:metabolism*; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000037:antagonists & inhibitors / Q000378:metabolism*
D019253:Proto-Oncogene Proteins c-bcl-2