Lipidic pore formation by the concerted action of proapoptotic BAX and tBID

被引:193
作者
Terrones, O
Antonsson, B
Yamaguchi, H
Wang, HG
Liu, JH
Lee, RM
Herrmann, A
Basañez, G
机构
[1] Univ Basque Country, Euskal Herriko Unibertsitatea, Ctr Mixto, CSIC,Unidad Biofis, E-48080 Bilbao, Spain
[2] Serono Int SA, Serono Pharmaceut Res Inst, CH-1228 Geneva, Switzerland
[3] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Drug Discovery Program, Tampa, FL 33612 USA
[4] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA
[5] Univ Utah, Dept Internal Med, Salt Lake City, UT 84112 USA
[6] Univ Utah, Dept Oncol Sci, Salt Lake City, UT 84112 USA
[7] Humboldt Univ, Inst Biol Mol Biophys, D-10115 Berlin, Germany
关键词
D O I
10.1074/jbc.M313420200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BCL-2 homology 3 (BH3)-only proteins of the BCL-2 family such as tBID and BIMEL assist BAX-type proteins to breach the permeability barrier of the outer mitochondrial membrane, thereby allowing cytoplasmic release of cytochrome c and other active inducers of cell death normally confined to the mitochondrial intermembrane space. However, the exact mechanism by which tBID and BIMEL aid BAX and its close homologues in this mitochondrial protein release remains enigmatic. Here, using pure lipid vesicles, we provide evidence that tBID acts in concert with BAX to 1) form large membrane openings through both BH3-dependent and BH3-independent mechanisms, 2) cause lipid trans-bilayer movement concomitant with membrane permeabilization, and 3) disrupt the lipid bilayer structure of the membrane by promoting positive monolayer curvature stress. None of these effects were observed with BAX when BIMEL was substituted for tBID. Based on these data, we propose a novel model in which tBID assists BAX not only via protein-protein but also via protein-lipid interactions to form lipidic pore-type nonbilayer structures in the outer mitochondrial membrane through which intermembrane prodeath molecules exit mitochondria during apoptosis.
引用
收藏
页码:30081 / 30091
页数:11
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