Dominant-negative c-Jun promotes neuronal survival by reducing BIM expression and inhibiting mitochondrial cytochrome c release

Neuron

Volumn 29, Issue 3, 2001, Pages 629-643

  Whitfield, Jonathan ^a   Neame, Stephen J ^a   Paquet, Luc ^b   Bernard, Ora ^c   Ham, Jonathan ^a  

^a UNIVERSITY COLLEGE LONDON   (United Kingdom)

^b MCGILL UNIVERSITY   (Canada)

^c ROYAL MELBOURNE HOSPITAL   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

ANTISENSE OLIGONUCLEOTIDE; BIM PROTEIN; CASPASE; CYTOCHROME C; MEMBRANE PROTEIN; MESSENGER RNA; NERVE GROWTH FACTOR; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL SURVIVAL; CELL VIABILITY; CONTROLLED STUDY; ENZYME ACTIVATION; KNOCKOUT MOUSE; MITOCHONDRIAL MEMBRANE; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN LOCALIZATION; PROTEIN SECRETION; RAT; SYMPATHETIC NERVE CELL;

EID: 0035049449     PISSN: 08966273     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0896-6273(01)00239-2     Document Type: Article

References (60)

1. p53 is essential for developmental neuron death as regulated by the TrkA and p75 neurotrophin receptors
2. Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation
3. Induction of apoptosis by the transcription factor c-Jun
4. Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity
5. Temporal analysis of events associated with programmed cell death (apoptosis) of sympathetic neurons deprived of nerve growth factor
6. BAX is required for neuronal death after trophic factor deprivation and during development
7. Placement of the BCL2 family member BAX in the death pathway of sympathetic neurons activated by trophic factor deprivation
8. Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis
9. Evidence of a novel event during neuronal death: Development of competence-to-die in response to cytoplasmic cytochrome c
10. Genetic and metabolic status of NGF-deprived sympathetic neurons saved by an inhibitor of ICE family proteases
11. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition
12. Characterization of apoptosis in cultured rat sympathetic neurons after nerve growth factor withdrawal
13. Role of the Jun kinase pathway in the regulation of c-Jun expression and apoptosis in sympathetic neurons
14. Mechanisms and functions of cell death
15. Altered gene expression in neurons during programmed cell death: Identification of c-jun as necessary for neuronal apoptosis
16. Stress-induced Fas ligand expression in T cells is mediated through a MEK kinase 1-regulated response element in the Fas ligand promoter
17. bcl-2 transgene expression can protect neurons against developmental and induced cell death
18. Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene
19. Manipulation of adenovirus vectors
20. Role of BCL-2 in the survival and function of developing and mature sympathetic neurons
21. BCL-2 family members and the mitochondria in apoptosis
22. A c-Jun dominant-negative mutant protects sympathetic neurons against programmed cell death
23. c-Jun and the transcriptional control of neuronal apoptosis
24. BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with diverse antiapoptotic Bcl-2 members
25. Programmed cell death in animal development
26. c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release
27. Bax directly induces release of cytochrome c from isolated mitochondria
28. A simple and efficient method for purification of infectious recombinant adenovirus
29. DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NF-kappa B and AP-1
30. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
31. Withdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell death
32. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
33. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
34. Induction of apoptotic program in cell-free extracts: Requirement for dATP and cytochrome c
35. Transformation suppressor activity of a Jun transcription factor lacking its activation domain
36. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
37. Inhibitors of protein synthesis and RNA synthesis prevent neuronal death caused by nerve growth factor deprivation
38. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria
39. Blocking cytochrome c activity within intact neurons inhibits apoptosis
40. Bim: A novel member of the Bcl-2 family that promotes apoptosis
41. An essential role for Rho, Rac, and Cdc42 GTPases in cell cycle progression through G1
42. Cell death during development of the nervous system
43. Neuronal cell death
44. Growth, purification and titration of adenoviruses
45. BAX translocation is a critical event in neuronal apoptosis: Regulation by neuroprotectants, BCL-2, and caspases
46. The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex
47. Programmed cell death of embryonic motoneurons triggered through the Fas death receptor
48. The role of Jun transcription factor expression and phosphorylation in neuronal differentiation, neuronal cell death, and plastic adaptations in vivo
49. p53 induces apoptosis by caspase activation through mitochondrial cytochrome c release
50. Apoptosis in neurodegenerative disorders
51. Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway
52. Bax promotes neuronal cell death and is downregulated during the development of the nervous system
53. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
54. Bid: A novel BH3 domain-only death agonist
55. Phosphorylation of c-Jun is necessary for apoptosis induced by survival signal withdrawal in cerebellar granule neurons
56. The anti-apoptotic protein ITA is essential for NGF-mediated survival of embryonic chick neurons
57. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death
58. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
59. Apoptosis in the nervous system