期刊
CELL CYCLE
卷 7, 期 1, 页码 39-44出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.7.1.5178
关键词
Bax; Bak; Bcl-2; pro-survival; apoptosis; BH3
类别
资金
- NCI NIH HHS [CA80188, CA43540] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA043540, R01CA080188] Funding Source: NIH RePORTER
In spite of the available genetic, biochemical and structural data, precisely how the initiators of apoptosis, the BH3-only proteins, trigger Bax and Bak to cause organellar damage remains highly contentious. A widely accepted model suggests that these two critical mediators of apoptosis remain inert until they are directly activated by a subclass of BH3-only proteins including Bim, Bid, and possibly Puma. However, our recent work showed that these death ligands are dispensable for apoptosis to proceed, whereas neutralization of the pro-survival Bcl-2 proteins is essential. These findings challenge current assumptions about how the BH3-only proteins provoke apoptotic cell death and have implications for the development of therapeutics to interfere with the Bcl-2 regulated apoptotic pathway for treating diseases such as cancer.
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