Early transitory rise in intracellular pH leads to Bax conformation change during ceramide-induced apoptosis

Apoptosis

Volumn 5, Issue 6, 2000, Pages 551-560

  Belaud Rotureau, M A ^a,b   Leducq, N ^c   De Gannes, F Macouillard Poulletier ^c   Diolez, P ^c   Lacoste, L ^a   Lacombe, F ^a   Bernard, P ^a,b   Belloc, F ^a,b  

^a HAUT LÉVÊQUE HOSPITAL   (France)

^b UNIVERSITÉ DE BORDEAUX   (France)

^c CNRS University Bordeaux Segalen   (France)

Author keywords

Apoptosis; Bax; Ceramide; Mitochondria; pH

Indexed keywords

CASPASE; CERAMIDE; FAS ANTIGEN; PROTEIN BAX;

APOPTOSIS; ARTICLE; CELL LABELING; CELL PH; CONFORMATIONAL TRANSITION; CONTROLLED STUDY; ENZYME ACTIVATION; FLOW CYTOMETRY; HEMATOPOIETIC CELL; HUMAN; HUMAN CELL; IMMUNOREACTIVITY; MITOCHONDRION; PRIORITY JOURNAL; PROTEIN CONFORMATION;

EID: 0034483954     PISSN: 13608185     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1009693630664     Document Type: Article

References (54)

1. Social controls on cell survival and cell death
2. Apoptosis and disease: Regulation and clinical relevance of programmed cell death
3. Regulation of lymphocyte survival by the bcl-2 gene family
4. The role of the bcl-2/ced-9 gene family in cancer and general implications of defects in cell death control for tumourigenesis and resistance to chemotherapy
5. BCL-2 family: Regulators of cell death
6. Proapoptotic protein Bax heterodimerizes with Bcl-2 and homodimerizes with Bax via a novel domain (BH3) distinct from BH1 and BH2
7. Bcl-2 hererodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death
8. Apoptosis meets signal transduction: Elimination of a BAD influence
9. Role of mitochondria and C-terminal membrane anchor of Bcl-2 in Bax induced growth arrest and mortality in Sacchatomyces cerevisiae
10. Subcellular and submitochondrial mode of action of Bcl-2-like oncoproteins
11. Mitochondria and apoptosis
12. Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis
13. Withdrawal of IL-7 induces Bax translocation front cytosol to mitochondria through a rise in intracellular pH
14. Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3
15. X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death
16. Bcl-x(L) forms an ion channel in synthetic lipid membranes
17. Inhibition of Bax channel-forming activity by Bcl-2
18. Channel formation by antiapoptotic prorein Bcl-2
19. Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death
20. Sequential acquisition of mitochondrial and plasma membrane alterations during early lymphocyte apoptosis
21. Mitochondrial permeability transition is a central coordinating event of apoptosis
22. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
23. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
24. The Bcl-2 protein family: Arbiters of cell survival
25. Structure-function comparisons of the proapoptotic protein Bax in yeast and mammalian cells
26. Bax- and Bak-induced cell death in the fission yeast Schizosaccharomyces pombe
27. Functions of ceramide in coordinating cellular responses to stress
28. Tumor nectosis factor activation of the sphingomyelin pathway signals nuclear factor kappa B translocation in intact HL-60 cells
29. Role for ceramide as an endogenous mediator of Fas-induced cytotoxicity
30. The IL-1 receptor signaling pathway
31. Functional dichotomy of neutral and acidic sphingomyelinases in tumor necrosis factor signaling
32. On the complexities of ceramide changes in cells undergoing apoptosis: Lack of evidence for a second messenger function in apoptotic induction
33. Ceramide synthase mediates daunorubicin-induced apoptosis: An alternative mechanism for generating death signals
34. Ceramide-induced apoptosis occurs independently of caspases and is decreased by leupeptin
35. Flow cytometric analysis of mitochondrial activity in situ: Application to acetylceramide-induced mitochondrial swelling and apoptosis
36. Expression of p53 protein during the cell cycle measured by flow cytometry in human leukemia
37. Flow cytometry CD45 gating for immunophenotyping of acute myeloid leukemia
38. Caspase activation is an early event in anthracycline-induced apoptosis and allows detection of apoptotic cells before they are ingested by phagocytes
39. A flow cytometric method using Hoechst 33342 and ptopidium iodide for simultaneous cell cycle analysis and apoptosis determination in unfixed cells
40. Study of apoptosis-related responses of leukemic blast cells to in vitro anthracycline treatment
41. Bcr-abl translocation can occur during the induction of multidrug resistance and confers apoptosis resistance on myeloid leukemic cell lines
42. Measurement of intracellular pH in cultured cells by flow cytometry with BCECFAM
43. Activation of the Na(+)/H(+) antipotter, Na+/HCO3(-)/CO3(2-) cotransporter, or Cl(-)/HCO3(-) exchanger in spontaneous thymocyte apoptosis
44. Fluorescein conjugates as indicators of subcellular pH. A critical evaluation
45. Bax, but not bcl-2, influences the prognosis of human pancreatic cancer
46. Analysis of Bax and Bcl-2 expression in p53-immunopositive breast cancers
47. Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore
48. Effects of Na+/H+ antiport and intracellular pH in the regulation of HL-60 cell apoptosis
49. Apoptosis induced by IL-2 withdrawal is associated with an intracellular acidification
50. Biophysical characterization of the oligomeric state of Bax and its complex formation with Bcl-XL
51. Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis
52. The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol
53. Investigation of bax-induced release of cytochrome c from yeast mitochondria permeability of mitochondrial membranes, role of VDAC and ATP requirement
54. Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization