Bid induces cytochrome c-impermeable Bax channels in liposomes

Biochemical Journal

Volumn 363, Issue 3, 2002, Pages 547-552

  Roucou, Xavier ^a   Rostovtseva, Tatiana ^a   Montessuit, Sylvie ^a   Martinou, Jean Claude ^a   Antonsson, Bruno ^a  

^a SERONO PHARMACEUTICAL RES INSTITUTE   (Switzerland)

Author keywords

Apoptosis; Bax; Bid; Channel; Mitochondria; Oligomerization

Indexed keywords

CELLS; CYTOLOGY; LIPIDS; MONOMERS; POLYMERIZATION; PROTEINS;

MITOCHONDRIA;

BIOCHEMISTRY;

CASPASE 8; CYTOCHROME C; ION CHANNEL; LIPOSOME; MONOMER; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BCL XL; PROTEIN BID; RECOMBINANT ENZYME;

APOPTOSIS; ARTICLE; CARBOXY TERMINAL SEQUENCE; CHANNEL GATING; CONFORMATIONAL TRANSITION; ENZYME ACTIVATION; LIPID BILAYER; MEMBRANE PERMEABILITY; MEMBRANE VESICLE; OLIGOMERIZATION; OUTER MEMBRANE; PRIORITY JOURNAL; PROTEIN FAMILY; PROTEIN PROTEIN INTERACTION; PROTEIN PURIFICATION; PROTEIN TRANSPORT;

ANIMALS; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; BH3 INTERACTING DOMAIN DEATH AGONIST PROTEIN; CARRIER PROTEINS; CASPASE 8; CASPASE 9; CASPASES; CYTOCHROME C GROUP; ESCHERICHIA COLI; FLUORESCEINS; FLUORESCENT DYES; ION CHANNELS; LIPID BILAYERS; LIPOSOMES; MICE; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RECOMBINANT PROTEINS;

INSERTION SEQUENCES;

EID: 0036565774     PISSN: 02646021     EISSN: None     Source Type: Journal    
DOI: 10.1042/0264-6021:3630547     Document Type: Article

References (41)

1. An APAF-1 cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9
2. Cytochrome c and dATP-mediated oligomerization of Apaf-1 is a prerequisite for procaspase-9 activation
3. Caspase activation involves the formation of the apoptosome, a large (700 kDa) caspase-activating complex
4. Recruitment, activation and retention of caspase-9 and -3 by Apaf-1 apoptosome and associated XIAP complexes
5. Molecular characterization of mitochondrial apoptosis-inducing factor
6. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
7. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition
8. A serine protease, HtrA2, is released from the mitochondria and interacts with XIAP, inducing cell death
9. Mitochondria as the central control point of apoptosis
10. Breaking the mitochondrial barrier
11. X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death
12. Solution structure of BID, an intracellular amplifier of apoptotic signaling
13. Solution structure of the proapoptotio molecule BID: A structural basis for apoptotic agonists and antagonists
14. Structure of Bax: Coregulation of dimer formation and intracellular localization
15. Solution structure of the antiapoptotic protein bcl-2
16. Channel formation by antiapoptotic protein Bcl-2
17. Bcl-x(L) forms an ion channel in synthetic lipid membranes
18. Inhibition of Bax channel-forming activity by Bcl-2
19. Ion channel activity of the BH3 only Bcl-2 family member
20. BAX is required for neuronal death after trophic factor deprivation and during development
21. Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria
22. Movement of Bax from the cytosol to mitochondria during apoptosis
23. Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells
24. Bcl-2 prevents Bax oligomerization in the mitochondrial outer membrane
25. BAX-dependent transport of cytochrome c reconstituted in pure liposomes
26. Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane
27. tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
28. Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis
29. Expression and purification of full-length human Bax alpha
30. The destabilization of lipid membranes induced by the C-terminal fragment of caspase 8-cleaved bid is inhibited by the N-terminal fragment
31. Formation of bimolecular membranes from lipid monolayers and a study of their electrical properties
32. ATP transport through a single mitochondrial channel, VDAC, studied by current fluctuation analysis
33. BID: A novel BH3 domain-only death agonist
34. Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations
35. Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2
36. Nonionic detergents induce dimerization among members of the Bcl-2 family
37. Conformation of the Bax C-terminus regulates subcellular location and cell death
38. Bcl-xL promotes the open configuration of the voltage-dependent anion channel and metabolite passage through the outer mitochondrial membrane
39. Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis
40. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria
41. Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore