Controlling the cell death mediators Bax and Bak - Puzzles and conundrums
Author(s)
Fletcher, JI; Huang, DCS;
Details
Publication Year 2008-01-01, Volume 7, Issue #1, Page 39-44
Journal Title
CELL CYCLE
Publication Type
Journal Article
Abstract
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.
Publisher
LANDES BIOSCIENCE
Keywords
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 12:00:00
Last Modified: 0001-01-01 12:00:00
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