Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane

被引:1001
作者
Eskes, R [1 ]
Desagher, S [1 ]
Antonsson, B [1 ]
Martinou, JC [1 ]
机构
[1] Ares Serono Int SA, Serono Pharmaceut Res Inst, CH-1228 Geneva, Switzerland
关键词
D O I
10.1128/MCB.20.3.929-935.2000
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
In many types of apoptosis, the proapoptotic protein Bax undergoes a change in conformation at the level of the mitochondria. This event always precedes the release of mitochondrial cytochrome c, which, in the cytosol, activates caspases through binding to Apaf-1. The mechanisms by which Bax triggers cytochrome c release are unknown. Here we show that following binding to the BH3-domain-only proapoptotic protein Bid, Bax oligomerizes and then integrates in the outer mitochondrial membrane, where it triggers cytochrome c release. Bax mitochondrial membrane insertion triggered by Bid may represent a key step in pathways leading to apoptosis.
引用
收藏
页码:929 / 935
页数:7
相关论文
共 46 条
[1]   The Bcl-2 protein family: Arbiters of cell survival [J].
Adams, JM ;
Cory, S .
SCIENCE, 1998, 281 (5381) :1322-1326
[2]   Inhibition of Bax channel-forming activity by Bcl-2 [J].
Antonsson, B ;
Conti, F ;
Ciavatta, A ;
Montessuit, S ;
Lewis, S ;
Martinou, I ;
Bernasconi, L ;
Bernard, A ;
Mermod, JJ ;
Mazzei, G ;
Maundrell, K ;
Gambale, F ;
Sadoul, R ;
Martinou, JC .
SCIENCE, 1997, 277 (5324) :370-372
[3]   Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization [J].
Bossy-Wetzel, E ;
Newmeyer, DD ;
Green, DR .
EMBO JOURNAL, 1998, 17 (01) :37-49
[4]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[5]   A CONSERVED DOMAIN IN BAK, DISTINCT FROM BH1 AND BH2, MEDIATES CELL-DEATH AND PROTEIN-BINDING FUNCTIONS [J].
CHITTENDEN, T ;
FLEMINGTON, C ;
HOUGHTON, AB ;
EBB, RG ;
GALLO, GJ ;
ELANGOVAN, B ;
CHINNADURAI, G ;
LUTZ, RJ .
EMBO JOURNAL, 1995, 14 (22) :5589-5596
[6]   Solution structure of BID, an intracellular amplifier of apoptotic signaling [J].
Chou, JJ ;
Li, HL ;
Salvesen, GS ;
Yuan, JY ;
Wagner, G .
CELL, 1999, 96 (05) :615-624
[7]   BAX is required for neuronal death after trophic factor deprivation and during development [J].
Deckwerth, TL ;
Elliott, JL ;
Knudson, CM ;
Johnson, EM ;
Snider, WD ;
Korsmeyer, SJ .
NEURON, 1996, 17 (03) :401-411
[8]   Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis [J].
Desagher, S ;
Osen-Sand, A ;
Nichols, A ;
Eskes, R ;
Montessuit, S ;
Lauper, S ;
Maundrell, K ;
Antonsson, B ;
Martinou, JC .
JOURNAL OF CELL BIOLOGY, 1999, 144 (05) :891-901
[9]   Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ions [J].
Eskes, R ;
Antonsson, B ;
Osen-Sand, A ;
Montessuit, S ;
Richter, C ;
Sadoul, R ;
Mazzei, G ;
Nichols, A ;
Martinou, JC .
JOURNAL OF CELL BIOLOGY, 1998, 143 (01) :217-224
[10]   Bcl-2 prevents activation of CPP32 cysteine protease and cleavage of poly (ADP-ribose) polymerase and U1-70 kD proteins in staurosporine-mediated apoptosis [J].
Estoppey, S ;
Rodriguez, I ;
Sadoul, R ;
Martinou, JC .
CELL DEATH AND DIFFERENTIATION, 1997, 4 (01) :34-38