Mitochondria as the central control point of apoptosis

被引：1795
作者：
Desagher, S
Martinou, JC
机构：
[1] CCIPE, CNRS 9023, UPR, F-34094 Montpellier 5, France
[2] Serono Pharmaceut Res Inst, CH-1228 Geneva, Switzerland
来源：
TRENDS IN CELL BIOLOGY | 2000年 / 10卷 / 09期
关键词：
D O I：
10.1016/S0962-8924(00)01803-1
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Mitochondria play a major role in apoptosis triggered by many stimuli. They integrate death signals through Bcl-2 family members and coordinate caspase activation through the release of cytochrome c as a result of the outer mitochondrial membrane becoming permeable. The mechanisms that lead to this permeability are not yet completely understood. Here, we attempt to summarize our current view of the mechanisms that lead to the efflux of many proteins from mitochondria during apoptosis and the role played by Bcl-2 family proteins in the control of this event.
引用
收藏
页码：369 / 377
页数：9
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共 69 条
  • [1] An emerging blueprint for apoptosis in Drosophila
    Abrams, JM
    [J]. TRENDS IN CELL BIOLOGY, 1999, 9 (11) : 435 - 440
  • [2] Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria
    Antonsson, B
    Montessuit, S
    Lauper, S
    Eskes, R
    Martinou, JC
    [J]. BIOCHEMICAL JOURNAL, 2000, 345 : 271 - 278
  • [3] Inhibition of Bax channel-forming activity by Bcl-2
    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
    [J]. SCIENCE, 1997, 277 (5324) : 370 - 372
  • [4] Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations
    Basañez, G
    Nechushtan, A
    Drozhinin, O
    Chanturiya, A
    Choe, E
    Tutt, S
    Wood, KA
    Hsu, YT
    Zimmerberg, J
    Youle, RJ
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (10) : 5492 - 5497
  • [5] Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization
    Bossy-Wetzel, E
    Newmeyer, DD
    Green, DR
    [J]. EMBO JOURNAL, 1998, 17 (01) : 37 - 49
  • [6] Distinct stages of cytochrome c release from mitochondria: evidence for a feedback amplification loop linking caspase activation to mitochondrial dysfunction in genotoxic stress induced apoptosis
    Chen, Q
    Gong, B
    Almasan, A
    [J]. CELL DEATH AND DIFFERENTIATION, 2000, 7 (02) : 227 - 233
  • [7] Conversion of Bcl-2 to a Bax-like death effector by caspases
    Cheng, EHY
    Kirsch, DG
    Clem, RJ
    Ravi, R
    Kastan, MB
    Bedi, A
    Ueno, K
    Hardwick, JM
    [J]. SCIENCE, 1997, 278 (5345) : 1966 - 1968
  • [8] Solution structure of BID, an intracellular amplifier of apoptotic signaling
    Chou, JJ
    Li, HL
    Salvesen, GS
    Yuan, JY
    Wagner, G
    [J]. CELL, 1999, 96 (05) : 615 - 624
  • [9] The mitochondrial permeability transition pore and its role in cell death
    Crompton, M
    [J]. BIOCHEMICAL JOURNAL, 1999, 341 : 233 - 249
  • [10] The 55-kDa tumor necrosis factor receptor induces clustering of mitochondria through its membrane-proximal region
    De Vos, K
    Goossens, V
    Boone, E
    Vercammen, D
    Vancompernolle, K
    Vandenabeele, P
    Haegeman, G
    Fiers, W
    Grooten, J
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (16) : 9673 - 9680
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