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pubmed-article:12662143pubmed:abstractTextIt is likely that most, if not all, cancer cells possess a mechanism for opposing programmed cell death, or apoptosis. One mechanism often used by cancer cells to escape apoptosis is the overexpression of B cell leukaemia/lymphoma-2 protein (BCL-2) or related antiapoptotic proteins. Inhibiting BCL-2, therefore, is an anticancer strategy worthy of attention. BCL-2 homology 3 (BH3) domains are alpha-helical segments found in BCL-2 family member proteins. In pro-apoptotic members, the BH3 domain is necessary for pro-apoptotic function. It has been shown that short peptides derived from the BH3 region possess intrinsic pro-death activity. Furthermore, certain peptides of this group exert their pro-death function by specifically binding BCL-2 and opposing BCL-2's antideath function. Therefore, BH3 domains are prototype BCL-2 inhibitors. Mimetics of BH3 domains, whether derived from peptides or small molecules, have promise as cancer therapeutics.lld:pubmed
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pubmed-article:12662143pubmed:authorpubmed-author:LetaiAnthonyAlld:pubmed
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pubmed-article:12662143pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:12662143pubmed:year2003lld:pubmed
pubmed-article:12662143pubmed:articleTitleBH3 domains as BCL-2 inhibitors: prototype cancer therapeutics.lld:pubmed
pubmed-article:12662143pubmed:affiliationDana-Farber Cancer Institute, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA. anthony_letai@dfci.harvard.edulld:pubmed
pubmed-article:12662143pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12662143pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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