Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario

被引:462
作者
Chipuk, J. E. [1 ]
Bouchier-Hayes, L. [1 ]
Green, D. R. [1 ]
机构
[1] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA
关键词
apoptosis; mitochondria; BCL-2; proteins; BH3-only proteins; MOMP; membrane;
D O I
10.1038/sj.cdd.4401963
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
Mitochondrial outer membrane permeabilization ( MOMP) is considered the 'point of no return' as this event is responsible for engaging the apoptotic cascade in numerous cell death pathways. MOMP is directly governed by a subset of the BCL-2 family of proapoptotic proteins, which induce disruptions in the outer mitochondrial membrane ( OMM) and subsequent release of death-promoting proteins like cytochrome c. The proposal here is centered on our hypothesis that MOMP is dictated by an interaction between the cytosol and the OMM, and although proteins of the OMM may be important in the process, the 'decision' to undergo apoptosis originates within the cytosol with no participation (in terms of yes, no and when) by mitochondria.
引用
收藏
页码:1396 / 1402
页数:7
相关论文
共 62 条
  • [31] Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics
    Letai, A
    Bassik, MC
    Walensky, LD
    Sorcinelli, MD
    Weiler, S
    Korsmeyer, SJ
    [J]. CANCER CELL, 2002, 2 (03) : 183 - 192
  • [32] Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
    Li, HL
    Zhu, H
    Xu, CJ
    Yuan, JY
    [J]. CELL, 1998, 94 (04) : 491 - 501
  • [33] Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
    Li, P
    Nijhawan, D
    Budihardjo, I
    Srinivasula, SM
    Ahmad, M
    Alnemri, ES
    Wang, XD
    [J]. CELL, 1997, 91 (04) : 479 - 489
  • [34] Growth factor regulation of autophagy and cell survival in the absence of apoptosis
    Lum, JJ
    Bauer, DE
    Kong, M
    Harris, MH
    Li, C
    Lindsten, T
    Thompson, CB
    [J]. CELL, 2005, 120 (02) : 237 - 248
  • [35] Lum May-Ghee, 2002, ScientificWorldJournal, V2, P1198
  • [36] Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
    Luo, X
    Budihardjo, I
    Zou, H
    Slaughter, C
    Wang, XD
    [J]. CELL, 1998, 94 (04) : 481 - 490
  • [37] Cardiolipin provides specificity for targeting of tBid to mitochondria
    Lutter, M
    Fang, M
    Luo, X
    Nishijima, M
    Xie, XS
    Wang, XD
    [J]. NATURE CELL BIOLOGY, 2000, 2 (10) : 754 - 756
  • [38] The pro-apoptotic Bcl-2 family member tBid localizes to mitochondrial contact sites
    Lutter, M
    Perkins, GA
    Wang, XD
    [J]. BMC CELL BIOLOGY, 2001, 2 (1)
  • [39] Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak
    Majewski, N
    Nogueira, V
    Bhaskar, P
    Coy, PE
    Skeen, JE
    Gottlob, K
    Chandel, NS
    Thompson, CB
    Robey, RB
    Hay, N
    [J]. MOLECULAR CELL, 2004, 16 (05) : 819 - 830
  • [40] p53 has a direct apoptogenic role at the mitochondria
    Mihara, M
    Erster, S
    Zaika, A
    Petrenko, O
    Chittenden, T
    Pancoska, P
    Moll, UM
    [J]. MOLECULAR CELL, 2003, 11 (03) : 577 - 590