Controlling the cell death mediators Bax and Bak - Puzzles and conundrums
Publication Year 2008-01-01, Volume 7, Issue #1, Page 39-44
- Journal Title
- CELL CYCLE
- Publication Type
- Journal Article
- 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.
- LANDES BIOSCIENCE
- BCL-2 FAMILY-MEMBERS; OUTER MITOCHONDRIAL-MEMBRANE; BH3-ONLY PROTEINS; BH3 DOMAIN; CYTOCHROME-C; INTERACTING PROTEIN; PROSURVIVAL BCL-2; PROAPOPTOTIC BAX; INDUCE APOPTOSIS; OLIGOMERIZES BAK
- Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2008-01-01 12:00:00Last Modified: 0001-01-01 12:00:00