期刊
CELL DEATH AND DIFFERENTIATION
卷 16, 期 9, 页码 1187-1191出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2009.83
关键词
apoptosis; Bcl-2; Bax; Bim
资金
- Australian NHMRC,
- US NCI
- Leukemia and Lymphoma Society
- Cancer Council of Victoria
- Victorian State Government
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
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