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. 2009 Aug 10;186(3):355–362. doi: 10.1083/jcb.200905153

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© 2009 Mérino et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 5. — Model for the initiation of apoptosis by Bim. (A) In the absence of Bim, Bax is kept in check by both subsets of its prosurvival relatives (“Bcl” represents Bcl-2, Bcl-x_L, and Bcl-w; “Mcl” represents Mcl-1 and A1; Willis et al., 2007). (B) In cells expressing Bim^Bad, the Bcl subset is neutralized, but the Mcl subset still partially restrains Bax and limits its induction of apoptosis. Conversely, in Bim^Noxa mice, Bax is partly restrained by the Bcl proteins. (C) In mice expressing Bim^Puma, all of the prosurvival proteins are neutralized, allowing the unrestrained Bax to induce very substantial apoptosis. (D) Unlike the three Bim BH3 mutants, WT Bim is proposed to also bind transiently to Bax, giving maximal activity.