[摘要]：Proteins of the Bcl-2 family regulate programmed cell death in mammals by promoting the release of cytochrome c from mitochondria in response to various proapoptotic stimuli. The mechanism by which BH3-only members of the family activate multidomain proapoptotic proteins Bax and Bak to form a pore in mitochondrial membranes remains under dispute. We report that cell death promoting activity of BH3-only protein Bim can be reconstituted in yeast when both Bax and antiapoptotic protein Bcl-X-L are present, suggesting that Bim likely activates Bax indirectly by inhibiting antiapoptotic proteins. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
