The combination of Bcl-2 expression and NGF-deprivation facilitates the selective destruction of BAD protein in living sympathetic neurons

Molecular and Cellular Neurosciences

Volumn 16, Issue 2, 2000, Pages 97-110

  Roberts, Michael L ^a   Virdee, Kanwar ^a   Sampson, Catherine P B ^a   Gordon, Ian ^b   Parone, Philippe ^c   Tolkovsky, Aviva M ^a  

^a UNIVERSITY OF CAMBRIDGE   (United Kingdom)

^b UNIVERSITY OF OXFORD   (United Kingdom)

^c NONE

Author keywords

[No Author keywords available]

Indexed keywords

NERVE GROWTH FACTOR; PROTEIN BAD; PROTEIN BCL 2;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BRAIN PROTECTION; CELL PROTECTION; CONTROLLED STUDY; GENE EXPRESSION REGULATION; NERVE CELL NECROSIS; NEWBORN; NONHUMAN; PRIORITY JOURNAL; RAT; SYMPATHETIC NERVE CELL;

ANIMALIA;

EID: 0033845480     PISSN: 10447431     EISSN: None     Source Type: Journal    
DOI: 10.1006/mcne.2000.0867     Document Type: Article

References (53)

1. Role of bcl-2 in the brain-derived neurotrophic factor survival response
2. The protooncogene bcl-2 can selectively rescue neurotrophic factor-dependent neurons from apoptosis
3. A role for MAPK/ERK in sympathetic neuron survival: Protection against a p53-dependent, JNK-independent induction of apoptosis by cytosine arabinoside
4. Protection of retinal ganglion cells from natural and axotomy-induced cell death in neonatal transgenic mice overexpressing bcl-2
5. Bcl-2 promotes regeneration of severed axons in mammalian CNS
6. Bcl2 overexpression reduces apoptotic photo-receptor death in three different retinal degenerations
7. Mitogen-activated protein kinase-independent pathways mediate the effects of nerve growth-factor and cAMP on neuronal survival
8. Phosphatidylinositol 3-kinase and Akt protein kinase are necessary and sufficient for the survival of nerve growth factor-dependent sympathetic neurons
9. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
10. Bax is required for neuronal death after trophic factor deprivation and during development
11. Temporal analysis of events associated with programmed cell-death (apoptosis) of sympathetic neurons deprived of nerve growth-factor
12. Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt
13. Genetic and metabolic status of ngf-deprived sympathetic neurons saved by an inhibitor of ICE family proteases
14. Neonatal motoneurons overexpressing the bcl-2 protooncogene in transgenic mice are protected from axotomy-induced cell-death
15. Analysis of events leading to neuronal death after infection with E1-deficient adenoviral vectors
16. Characterization of apoptosis in cultured rat sympathetic neurons after nerve growth-factor withdrawal
17. Role of the Jun kinase pathway in the regulation of c-Jun expression and apoptosis in sympathetic neurons
18. Bcl-2 transgene expression can protect neurons against developmental and induced cell-death
19. Prevention of programmed cell death of sympathetic neurons by the bcl-2 protooncogene
20. Methods for construction of adenovirus vectors
21. Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A
22. Interference of BAD (BcL-xL/BcL-2-associated death promoter)-induced apoptosis in mammalian cells by 14-3-3 isoforms and P11
23. Bad is a BH3 domain-containing protein that forms an inactivating dimer with BcL-x(L)
24. Bcl-2 family proteins: The role of the BH3 domain in apoptosis
25. The release of cytochrome c from mitochondria: A primary site for BcL-2 regulation of apoptosis
26. Bcl-2 and Bax function independently to regulate cell death
27. Altered cytokine export and apoptosis in mice deficient in interleukin 1beta converting enzyme
28. E40rf4,a novel adenovirus death factor that induces p53-independent apoptosis by a pathway that is not inhibited by zVAD-fmk
29. Emergence of early region-1-containing replication-competent adenovirus in stocks of replication-defective adenovirus recombinants (delta-E1 plus delta-E3) during multiple passages in 293-cells
30. BCL-2-related protein expression in apoptosis: Oxidative stress versus serum deprivation in PC12 cells
31. Overexpression of Bcl-2 in transgenic mice protects neurons from naturally occurring cell-death and experimental-ischemia
32. A simple technique for the rescue of early region 1 mutations into infectious human adenovirus
33. Bcl-2 gene family in the nervous system
34. Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development
35. Bcl2 accelerates the maturation of early sensory neurons
36. BclxL regulated apoptosis by heterodimerisation-dependent and -independent mechanisms
37. Dimerisation properties of human BAD
38. Ordering the cell death pathway - Differential effects of BCL2, an interleukin-1-converting enzyme family protease inhibitor, and other survival agents on JNK activation in serum nerve growth factor-deprived PC12 cells
39. Bcl-2 family proteins
40. Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c
41. A novel strategy for introducing exogenous Bcl-2 into neuronal cells: The cre/loxP system-mediated activation of Bcl-2 for preventing programmed cell death using recombinant adenoviruses
42. Non-specific effects of methyl ketone peptide inhibitors of caspases
43. Cloning of the herpes-simplex virus icp4 gene in an adenovirus vector-effects on adenovirus gene-expression and replication
44. Comparison between the timing of JNK activation, c-Jun phosphorylation, and onset of death commitment in sympathetic neurones
45. Activation of p44 and p42 MAP kinases is not essential for the survival of rat sympathetic neurons
46. Inhibition of p42 and p44 mitogen-activated protein-kinase activity by PD98059 does not suppress nerve growth factor-induced survival Of sympathetic neurons
47. NGF-induced PKB/Akt activity is sutained by phosphoinositide 3-kinase dependent and independent signals in sympathetic neurons
48. Murine caspase-11, and ICE-interacting protease, is essential for the activation of ICE
49. Prevention of apoptosis by Bcl2. Release of cytochrome c from mitochondria blocked
50. Bad, a heterodimeric partner for Bcl-xL and Bcl-2 displaces Bax and promotes cell death
51. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyride neurotoxicity is attenuated in mice overexpressing Bcl-2
52. BH3 domain of BAD is required for heterodimerization with BCL-X-L and pro-apoptotic activity
53. Apoptosis in human monocytic THP-1 cell results in the release of cytochrome c from mitochondria prior to their ultracondensation, formation of outer membrane discontinuities and reduction of inner membrane potential