Wild-type, mitochondrial and ER-restricted Bcl-2 inhibit DNA damage-induced apoptosis but do not affect death receptor-induced apoptosis

Journal of Cell Science

Volumn 114, Issue 23, 2001, Pages 4161-4172

  Rudner, J ^a   Lepple Wienhues, A ^a   Budach, W ^a   Berschauer, J ^a   Friedrich, B ^a   Wesselborg, S ^a   Schulze Osthoff, K ^a   Belka, C ^a  

^a UNIVERSITY OF TÜBINGEN   (Germany)

Author keywords

Apoptosis; Bcl 2; CD95; Endoplasmic reticulum; Mitochondria; Radiation

Indexed keywords

CASPASE; CELL RECEPTOR; CYTOCHROME B5; DNA; FAS ANTIGEN; MUTANT PROTEIN; PROTEIN BCL 2; TUMOR NECROSIS FACTOR RELATED APOPTOSIS INDUCING LIGAND;

APOPTOSIS; ARTICLE; CELL COMPARTMENTALIZATION; CELL ORGANELLE; CELL PROTECTION; CONTROLLED STUDY; DNA DAMAGE; ENDOPLASMIC RETICULUM; ENZYME ACTIVATION; GENE EXPRESSION; GENE INSERTION; HUMAN; HUMAN CELL; IONIZING RADIATION; LEUKEMIA CELL LINE; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; OUTER MEMBRANE; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN TARGETING; PROTO ONCOGENE; STIMULUS;

ANTIGENS, CD95; APOPTOSIS; APOPTOSIS REGULATORY PROTEINS; CASPASE 12; CASPASES; DNA DAMAGE; ENDOPLASMIC RETICULUM; HUMANS; JURKAT CELLS; MEMBRANE GLYCOPROTEINS; MITOCHONDRIA; PROTO-ONCOGENE PROTEINS C-BCL-2; RADIATION, IONIZING; SUBCELLULAR FRACTIONS; TNF-RELATED APOPTOSIS-INDUCING LIGAND; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0035211935     PISSN: 00219533     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (72)

1. Apoptosis induced by withdrawal of interleukin-3 (IL-3) from an IL-3-dependent hematopoietic cell line is associated with repartitioning of intracellular calcium and is blocked by enforced Bcl-2 oncoprotein production
2. Radiation-induced apoptosis in human lymphocytes and lymphoma cells critically relies on the up-regulation of CD95/Fas/APO-1 ligand
3. The tyrosine kinase lck is required for CD95-independent caspase-8 activation and apoptosis in response to ionizing radiation
4. Differential role of caspase-8 and BID activation during radiation- and CD95-induced apoptosis
5. Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity
6. Apoptosis induced by microinjection of cytochrome c is caspase-dependent and is inhibited by Bcl-2
7. Aven, a novel inhibitor of caspase activation, binds Bcl-xL and Apaf-1
8. Bax-independent inhibition of apoptosis by Bcl-XL
9. Interaction of CED-4 with CED-3 and CED-9: A molecular framework for cell death
10. The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9
11. Caspase-8/FLICE functions as an executioner caspase in anticancer drug-induced apoptosis
12. 2+ concentration within the endoplasmic reticulum
13. A conserved checkpoint pathway mediates DNA damage-induced apoptosis and cell cycle arrest in C. elegans
14. Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2
15. Differential requirement for caspase 9 in apoptotic pathways in vivo
16. Pro-apoptotic apoptosis protease-activating factor 1 (Apaf-1) has a cytoplasmic localization distinct from Bcl-2 or Bcl-x(L)
17. Maintenance of calcium homeostasis in the endoplasmic reticulum by Bcl-2
18. Bcl-XL interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation
19. Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-x(L)
20. Bcl-2 does not inhibit cell death induced by the physiological Fas ligand: Implications for the existence of type I and type II cells
21. T cells deficient in inositol 1,4,5-trisphosphate receptor are resistant to apoptosis
22. Bax directly induces release of cytochrome c from isolated mitochondria
23. 2+ excitability of the endoplasmic reticulum
24. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
25. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9
26. Bcl-2 targeted to the endoplasmic reticulum can inhibit apoptosis induced by Myc but not etoposide in Rat-1 fibroblasts
27. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
28. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
29. The protein product of the oncogene bcl-2 is a component of the nuclear envelope, the endoplasmic reticulum, and the outer mitochondrial membrane
30. p53 is required for radiation-induced apoptosis in mouse thymocytes
31. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
32. lck is required for ceramide-induced but not tumor necrosis factor-induced activation of NF-kappa B, AP-1, JNK, and apoptosis
33. Bcl-xL regulates apoptosis by heterodimerization-dependent and -independent mechanisms
34. Induction of apoptosis in fibroblasts by IL-1 beta-converting enzyme, a mammalian homolog of the C. elegans cell death gene ced-3
35. Bcl-2 family members do not inhibit apoptosis by binding the caspase activator Apaf-1
36. X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death
37. FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex
38. Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta
39. A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes
40. Ionizing radiation and chemotherapeutic drugs induce apoptosis in lymphocytes in the absence of Fas or FADD/MORT1 signaling. Implications for cancer therapy
41. p28 Bap31, a Bcl-2/Bcl-XL- and procaspase-8-associated protein in the endoplasmic reticulum
42. Bcl-XL cooperatively associates with the Bap31 complex in the endoplasmic reticulum, dependent on procaspase-8 and Ced-4 adaptor
43. Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis
44. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death
45. Caspase-9, Bcl-XL, and Apaf-1 from a ternary complex
46. Demonstration of the in vivo interaction of key cell death regulators by structure-based design of second-site suppressors
47. The overexpression of Bax produces cell death upon induction of the mitochondrial permeability transition
48. 2+ influx in Bcl-2-overexpressing cells
49. High tide of calcium in mitochondria
50. Radiation and stress-induced apoptosis: A Role for Fas/Fas ligand interactions
51. Radiation sensitivity and apoptosis in human lymphoma cells
52. Structure of Bcl-xL-Bak peptide complex: Recognition between regulators of apoptosis
53. Two CD95 (APO-1/Fas) signaling pathways
54. Differences between CD95 type I and II cells detected with the CD95 ligand
55. Multiple Bcl-2 family members demonstrate selective dimerizations with Bax
56. Interaction between the C. elegans cell-death regulators CED-9 and CED-4
57. Bcl-2 and Bcl-X(L) block thapsigargin-induced nitric oxide generation, c-Jun NH(2)-terminal kinase activity, and apoptosis
58. Pro-caspase-3 is a major physiologic target of caspase-8
59. Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis
60. Genetic evidence for the involvement of the lck tyrosine kinase in signal transduction through the T cell antigen receptor
61. Effects of intracellular calcium chelator BAPTA-AM on radiation-induced apoptosis regulated by activation of SAPK/JNK and caspase-3 in MOLT-4 cells
62. Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange
63. Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria
64. 2+ in radiation-induced apoptosis suppresses DNA fragmentation but does not enhance clonogenic survival
65. BID: A novel BH3 domain-only death agonist
66. Interaction and regulation of the Caenorhabditis elegans death protease CED-3 by CED-4 and CED-9
67. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
68. Essential role of CED-4 oligomerization in CED-3 activation and apoptosis
69. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
70. Apaf1 is required for mitochondrial pathways of apoptosis and brain development
71. Bcl-2 mutants with restricted subcellular location reveal spatially distinct pathways for apoptosis in different cell types
72. Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3