Bax activation by Bim?
- Author(s)
- Czabotar, PE; Colman, PM; Huang, DCS;
- Details
- Publication Year 2009-09,Volume 16,Issue #9,Page 1187-1191
- Journal Title
- CELL DEATH AND DIFFERENTIATION
- Publication Type
- Journal Article
- Abstract
- The mechanism by which the cell death mediator Bax becomes activated to cause mitochondrial damage, a key step for the intrinsic pathway to apoptosis, remain highly contentious. Although some data support a role for certain BH3-only proteins, such as Bim or tBid, to directly activate Bax, others have led to the conclusion that BH3-only proteins act indirectly by antagonizing the prosurvival Bcl-2 proteins, thereby allowing Bax activation to proceed. A recent paper in Nature by Gavathiotis et al. provides the first biophysical evidence for a direct interaction between a BH3 domain, that of Bim, with Bax. Here, we review these intriguing observations and discuss their implications for our understanding of how the BH3-only proteins initiate apoptosis. Cell Death and Differentiation (2009) 16, 1187-1191; doi: 10.1038/cdd.2009.83; published online 26 June 2009
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- BCL-2 FAMILY-MEMBERS; BH3-ONLY PROTEINS; MEMBRANE PERMEABILIZATION; BH3 DOMAINS; CELL-DEATH; MITOCHONDRIAL APOPTOSIS; X-RAY; BINDING; HELIX; SITE
- Publisher's Version
- https://doi.org/10.1038/cdd.2009.83
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2009-09-01 12:00:00