Failure of Bcl-2 family members to interact with Apaf-1 in normal and apoptotic cells

Cell Death and Differentiation

Volumn 7, Issue 10, 2000, Pages 947-954

  Conus, S ^a,b   Rosse T ^a   Borner, C ^a,b  

^a UNIVERSITY OF FRIBOURG   (Switzerland)

^b UNIVERSITY OF FREIBURG   (Germany)

Author keywords

Apaf 1; Apoptosis; Bax; Bcl 2; Bcl x(L); CED 4

Indexed keywords

CASPASE 3; CYTOPLASM PROTEIN; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BCL X;

APOPTOSIS; ARTICLE; CAENORHABDITIS ELEGANS; CELL DEATH; CELL NUCLEUS; CONTROLLED STUDY; CYTOPLASM; ENZYME ACTIVATION; ENZYME BINDING; HUMAN; HUMAN CELL; IMMUNOFLUORESCENCE; IMMUNOPRECIPITATION; INTRACELLULAR MEMBRANE; MAMMAL; NEMATODE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN LOCALIZATION; PROTEIN PROTEIN INTERACTION; PROTEIN TARGETING; WESTERN BLOTTING;

ANIMAL; APOPTOSIS; CELLS, CULTURED; HUMAN; KIDNEY; PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RATS; SUPPORT, NON-U.S. GOV'T; TRANSFECTION;

EID: 0033774569     PISSN: 13509047     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.cdd.4400729     Document Type: Article

References (46)

1. Bcl-x(L) interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation
2. Caspase-9, Bcl-x(L), and Apaf-1 form a ternary complex
3. Bcl-2 family members do not inhibit apoptosis by binding the caspase activator Apaf-1
4. Cell death in development
5. Developing Caenorhabditis elegans neurons may contain both cell-death protective and killer activities
6. Interaction of CED-4 with CED-3 and CED-9: A molecular framework for cell death
7. Interaction and regulation of the C. Elegans death protease CED-3 by CED-4 and CED-9
8. Role of CED-4 in the activation of CED-3
9. Caenorhabditis elegans CED-4 stimulates CED-3 processing and CED-3-induced apoptosis
10. Essential role of CED-4 oligomerization in CED-3 activation and apoptosis
11. CED-4 is a stranger no more
12. Mammalian caspases: Structure, activation, substrates, and functions during apoptosis
13. Caspase structure, proteolytic substrates, and function during apoptotic cell death
14. Mechanisms mediating caspase activation in cell death
15. Apaf-1, a human protein homologous to C. Elegans CED-4, participates in cytochrome c-dependent activation of caspases
16. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
17. Autoactivation of procaspase-9 by Apaf-1-mediated oligomerization
18. Caspase activation involves the formation of the aposome, a large (700 kDa) caspase-activating complex
19. Apaf-1 and the apoptotic machinery
20. Role of cytochrome c and dATP/ATP hydrolysis in Apaf-1-mediated caspase-9 activation and apoptosis
21. Mitochondria and apoptosis
22. The Bcl-2 protein family: Arbiters of cell survival
23. Bcl-2 family proteins
24. Bcl-2 family proteins: The role of the BH3 domain in apoptosis
25. Bcl-2 overexpression blocks activation of the death protease CPP32/Yama/Apopain
26. Molecular Ordering of the cell death pathway: Bcl-2 and Bcl-xL function upstream of the CED-3-like apoptotic proteases
27. Bcl-2 and adenovirus E1B 19kDA protein prevent E1A-induced processing of CPP32 and cleavage of poly(ADP-ribose) polymeras
28. Interaction and regulation of subcellular localization of CED-4 by CED-9
29. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
30. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
31. Role for Bcl-xL as an inhibitor of cytosolic cytochrome c accumulation in DNA damage-induced apoptosis
32. Bcl-x(L) forms an ion channel in synthetic lipid membranes
33. Channel formation by antiapoptotic protein Bcl-2
34. Bid, a Bcl-2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
35. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway to apoptosis
36. Nonionic detergents induce dimerization among members of the Bcl-2 family
37. The binding properties and biological activities of Bcl-2 and Bax in cells exposed to apoptotic stimuli
38. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
39. Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c
40. Bcl-2 expressed using a retroviral vector is localized primarily in the nuclear membrane and the endoplasmic reticulum of chicken embryo fibroblasts
41. Interaction between the C. Elegans cell-death regulators CED-9 and CED-4
42. Nod1, and Apaf-1-like activator of caspase-9 and nuclear factor-kB
43. Human CARD4 protein is a novel CED-4/Apaf-1 cell death family member that activates NF-kB
44. Pro-apoptotic apoptosis protease-activating factor 1 (Apaf-1) has a cytoplasmic localization distinct from Bcl-2 and Bcl-x(L)
45. Bcl-xL does not inhibit the function of apaf-1
46. Apoptotic protease activating factor (Apaf-1)-independent cell death suppression by Bcl-2