Mitochondria: Regulating the inevitable

Biochimie

Volumn 84, Issue 2-3, 2002, Pages 105-111

  Parone, P A ^a   James, D ^a   Martinou, J C ^a  

^a UNIVERSITY OF GENEVA   (Switzerland)

Author keywords

Apoptosis; Apoptosis inducing factor; Bcl 2; Calcium; Caspases; Cytochrome c; Mitochondria

Indexed keywords

APOPTOTIC PROTEASE ACTIVATING FACTOR 1; CALCIUM ION; CASPASE; CASPASE 10; CASPASE 2; CASPASE 3; CASPASE 8; CASPASE 9; CHELATING AGENT; CYCLOSPORIN A; CYTOCHROME C; ETHYLENE GLYCOL 1,2 BIS(2 AMINOPHENYL) ETHER N,N,N',N' TETRAACETIC ACID; PROTEIN; PROTEIN BAD; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BID; PROTEIN P53;

APOPTOSIS; CAENORHABDITIS ELEGANS; CANCER; CELL SURFACE; DEGENERATIVE DISEASE; DNA DAMAGE; DRUG EFFECT; HOMEOSTASIS; INHIBITION KINETICS; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; MOLECULAR DYNAMICS; MORPHOLOGY; NONHUMAN; PROTEIN FUNCTION; REVIEW; SIGNAL TRANSDUCTION; TISSUE;

EID: 0036479004     PISSN: 03009084     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0300-9084(02)01380-9     Document Type: Article

References (81)

1. Suicidal tendencies: Apoptotic cell death by caspase family proteinases
2. Four deaths and a funeral: From caspases to alternative mechanisms
3. Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis
4. Solution structure of the proapoptotic molecule BID: A structural basis for apoptotic agonists and antagonists
5. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
6. Bim: A novel member of the Bcl-2 family that promotes apoptosis
7. The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex
8. Induction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosis
9. PUMA, a novel proapoptotic gene, is induced by p53
10. Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis
11. Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3
12. Death signal-induced localization of p53 protein to mitochondria. A potential role in apoptotic signaling
13. Induction of apoptotic program in cell-free extracts: Requirement for dATP and cytochrome c
14. Bcl-X-L interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation
15. WD-40 repeat region regulates Apaf-1 self-association and procaspase- 9 activation
16. Role of cytochrome c and dATP/ATP hydrolysis in Apaf-1-mediated caspase-9 activation and apoptosis
17. Autoactivation of procaspase-9 by Apaf-1-mediated oligomerization
18. Regulation of apoptotic protease activating factor-1 oligomerization and apoptosis by the WD-40 repeat region
19. An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9
20. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
21. Caspase-9 and APAF-1 form an active holoenzyme
22. IAP family proteins - Suppressors of apoptosis
23. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition
24. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
25. Structural and biochemical basis of apoptotic activation by Smac/DIABLO
26. Molecular determinants of the caspase-promoting activity of Smac/DIABLO and its role in the death receptor pathway
27. Endonuclease G is an apoptotic DNase when released from mitochondria
28. Molecular characterization of mitochondrial apoptosis-inducing factor
29. Apoptosis-inducing factor (AIF): A ubiquitous mitochondrial oxidoreductase involved in apoptosis
30. Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death
31. Primers for mitochondrial DNA replication generated by endonuclease G
32. Mitochondrial endonuclease G is important for apoptosis in C. elegans
33. Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore
34. Bax directly induces release of cytochrome c from isolated mitochondria
35. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria
36. Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis
37. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
38. Bcl-x(L) regulates the membrane potential and volume homeostasis of mitochondria
39. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
40. Inhibition of Bax channel-forming activity by Bcl-2
41. Bcl-x(L) forms an ion channel in synthetic lipid membranes
42. Channel formation by antiapoptotic protein Bcl-2
43. Ion channel activity of the BH3 only Bcl-2 family member, BID
44. Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c
45. Bax and Bak coalesce into novel mitochondria-associated clusters during apoptosis
46. Full-length Bax ruptures planar phospholipid membranes at subnanomolar concentrations
47. Bax, but not Bcl-x(L), decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations
48. The destabilization of lipid membranes induced by the C-terminal fragment of caspase 8-cleaved bid is inhibited by the N-terminal fragment
49. Electrophysiological study of a novel large pore formed by Bax and the voltage-dependent anion channel that is permeable to cytochrome c
50. Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux
51. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
52. BH4 domain of antiapoptotic Bcl-2 family members closes voltage-dependent anion channel and inhibits apoptotic mitochondrial changes and cell death
53. The mitochondrial permeability transition pore and its role in cell death
54. Mitochondrial depolarization accompanies cytochrome c release during apoptosis in PC6 cells
55. Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator
56. Calcium induced release of mitochondrial cytochrome c by different mechanisms selective for brain versus liver
57. Calcium entry through L-type calcium channels causes mitochondrial disruption and chromaffin cell death
58. Apoptosis in factor-dependent haematopoietic cells is linked to calcium-sensitive mitochondrial rearrangements and cytoskeletal modulation
59. A subpopulation of mitochondria prevents cytosolic calcium overload in endothelial cells after cold ischemia/reperfusion
60. Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells
61. Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event
62. Heat shock protein 70 inhibits caspase-dependent and -independent apoptosis in Jurkat T cells
63. 2+
64. Integrating cytosolic calcium signals into mitochondrial metabolic responses
65. Modulation of mitochondrial Ca(2+) homeostasis by Bcl-2
66. Feedback inhibition of sodium/calcium exchange by mitochondrial calcium accumulation
67. Bcl-2 does not inhibit the permeability transition pore in mouse liver mitochondria
68. 2+ concentration within the endoplasmic reticulum
69. Overexpression of Bcl-2 suppresses the calcium activation of a mitochondrial megachannel
70. 2+-induced apoptosis through calcineurin dephosphorylation of BAD
71. The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol
72. The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event
73. Death commitment point is advanced by axotomy in sympathetic neurons
74. Mitochondria and cell death. Mechanistic aspects and methodological issues
75. Chloromethyltetramethylrosamine (Mitotracker Orange) induces the mitochondrial permeability transition and inhibits respiratory complex I. Implications for the mechanism of cytochrome c release
76. Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis
77. Cardiolipin provides specificity for targeting of tBid to mitochondria
78. The Bcl-2 protein family
79. BCL-2 family members and the mitochondria in apoptosis
80. Pro-caspase-8 is predominantly localized in mitochondria and released into cytoplasm upon apoptotic stimulation
81. Mitochondria: Execution central