Taxol induces apoptosis in cortical neurons by a mechanism independent of Bcl-2 phosphorylation

Journal of Neuroscience

Volumn 21, Issue 13, 2001, Pages 4657-4667

  Figueroa Masot, Xavier A ^a   Hetman, Michal ^a   Higgins, Matthew J ^a   Kokot, Niels ^a   Xia, Zhengui ^a  

^a UNIVERSITY OF WASHINGTON   (United States)

Author keywords

Akt; Apoptosis; Bcl 2; CEP 1347; Cortical neurons; ERK1 2; JNK; KT7515; N terminal c Jun kinase; Paclitaxel; Pl 3 kinase; SAPK; Taxol

Indexed keywords

PACLITAXEL;

APOPTOSIS; ARTICLE; BRAIN CELL; CELL VIABILITY; DRUG EFFECT; DRUG MECHANISM; HUMAN; HUMAN CELL; NERVE DEGENERATION; NEUROPROTECTION; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION;

EID: 0035399873     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.21-13-04657.2001     Document Type: Article

References (72)

1. The bcl-2 protein family: Arbiters of cell survival
2. Transient stimulation of the c-Jun-NH2-terminal kinase/activator protein 1 pathway and inhibition of extracellular signal-regulated kinase are early effects in paclitaxel-mediated apoptosis in human B lymphoblasts
3. Microtubule-damaging drugs triggered bcl2 phosphorylation-requirement of phosphorylation on both serine-70 and serine-87 residues of bcl2 protein
4. Molecular effects of paclitaxel: Myths and reality
5. Taxol-induced apoptosis and phosphorylation of Bcl-2 protein involves c-Raf-1 and represents a novel c-Raf-1 signal transduction pathway
6. c-Jun NH2-terminal kinase regulation of the apoptotic response of small cell lung cancer cells to ultraviolet radiation
7. Identification of a novel regulatory domain in Bcl-X(L) and Bcl-2
8. Persistent activation of c-Jun N-terminal kinase 1 (JNK1) in gamma radiation-induced apoptosis
9. The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation: Duration of JNK activation may determine cell death and proliferation
10. Human cytomegalovirus iel transactivates the α promoter-enhancer via an 18-base-pair repeat element
11. Dual roles for c-Jun N-terminal kinase in developmental and stress responses in cerebellar granule neurons
12. Phosphatidylinositol 3-kinase and Akt protein kinase are necessary and sufficient for the survival of nerve growth factor-dependent sympathetic neurons
13. The survival of sympathetic neurons promoted by potassium depolarization, but not by cyclic AMP, requires phosphatidylinositol 3-kinase and Akt
14. The Bcl-2 family of proteins, and the regulation of neuronal survival
15. Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt
16. JNK1: A protein kinase stimulated by UV light and HA-ras binds to and activates the c-jun activation domain
17. Insulin-like growth factor and potassium depolarization maintain neuronal survival by distinct pathways: Possible involvement of PI 3-kinase in IGF-1 signaling
18. Regulation of neuronal survival by the serine-threonine protein kinase Akt
19. Vinblastine-induced phosphorylation of Bcl-2 and Bcl-XL is mediated by JNK and occurs in parallel with inactivation of the Raf-1/MEK/ERK cascade
20. "Loop" domain is necessary for taxol-induced mobility shift and phosphorylation of Bcl-2 as well as for inhibiting taxol-induced cytosolic accumulation of cytochrome c and apoptosis
21. The c-Jun N-terminal kinase cascade plays a role in stress-induced apoptosis in Jurkat cells by up-regulating Fas ligand expression
22. PI3K: Downstream AKTion blocks apoptosis
23. Inactivation of Bcl-2 by phosphorylation
24. Taxol induces bcl-2 phosphorylation and death of prostate cancer cells
25. Bcl2 is the guardian of microtubule integrity
26. Serine-70 is one of the critical sites for drug-induced Bcl2 phosphorylation in cancer cells
27. Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill
28. Neuroprotection by brain-derived neurotrophic factor is mediated by extracellular-signal-regulated kinase and phosphatidylinositol-3 kinase
29. Role of glycogen synthase kinase-3β in neuronal apoptosis induced by trophic withdrawal
30. MKK7 is a stress-activated mitogen-activated protein kinase kinase functionally related to hemipterous
31. Ras-dependent induction of cellular responses by constitutively active phosphatidylinositol-3 kinase
32. Mitotic block induced in HeLa cells by low concentrations of paclitaxel (taxol) results in abnormal mitotic exit and apoptotic cell death
33. The Jnk1 and Jnk2 protein kinases are required for regional specific apoptosis during early brain development
34. Cytotoxic effects of cell cycle phase specific agents: Result of cell cycle perturbation
35. Paclitaxel (taxol)-induced gene expression and cell death are both mediated by the activation of c-Jun NH2-terminal kinase (JNK/SAPK)
36. Withdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell death
37. Phosphorylation of Bcl-2 is a marker of M phase events and not a determinant of apoptosis
38. Dopamine induces apoptosis through an oxidation-involved SAPK/JNK activation pathway
39. MEK inhibition enhances paclitaxel-induced tumor apoptosis
40. Motoneuron apoptosis is blocked by CEP-1347 (KT 7515), a novel inhibitor of the JNK signaling pathway
41. CEP-1347 (KT7515), an inhibitor of JNK activation, rescues sympathetic neurons and neuronally differentiated PC12 cells from death evoked by three distinct insults
42. Effects of microtubule stabilization and destabilization on tau immunoreactivity in cultured hippocampal neurons
43. Bcl-2 undergoes phosphorylation by c-Jun N-terminal kinase/ stress-activated protein kinases in the presence of the constitutively active GTP-binding protein Racl
44. Protection against beta-amyloid toxicity in primary neurons by paclitaxel (taxol)
45. Inhibition of phosphatidylinositol 3-kinase activity blocks depolarization- and insulin-like growth factor I-mediated survival of cerebellar granule cells
46. Induction of neuronal apoptosis by camptothecin, an inhibitor of DNA topoisomerase-I: Evidence for cell cycle-independent toxicity
47. Arsenite-induced apoptosis in cortical neurons is mediated by c-Jun N-terminal protein kinase 3 and p38 mitogen-activated protein kinase
48. 1/S cell cycle blockers and inhibitors of cyclin-dependent kinases suppress camptothecin-induced neuronal apoptosis
49. Cyclin-dependent kinases participate in death of neurons evoked by DNA-damaging agents
50. Activation of c-Jun N-terminal kinase antagonizes an anti-apoptotic action of Bcl-2
51. The pathobiology of traumatically induced axonal injury in animals and humans: A review of current thoughts
52. Axonal dystrophy as a consequence of long-term demyelination
53. Transformation by raf and other oncogenes renders cells differentially sensitive to growth inhibition by a dominant negative c-jun mutant
54. Involvement of stress-activated protein kinase in the cellular response to 1-beta-D-arabinofuranosylcytosine and other DNA-damaging agents
55. Mitotic phosphorylation of Bcl-2 during normal cell cycle progression and taxol-induced growth arrest
56. c-Jun NH2-terminal kinase-mediated activation of interleukin-1 beta converting enzyme/CED-3-like protease during anticancer drug-induced apoptosis
57. Deletion of the loop region of Bcl-2 completely blocks paclitaxel-induced apoptosis
58. Axonal transection in the lesions of multiple sclerosis
59. Nedd2 is required for apoptosis after trophic factor withdrawal, but not superoxide dismutase (SOD1) downregulation, in sympathetic neurons and PC12 cells
60. Bcl-2 proteins: Regulators of apoptosis or of mitochondrial homeostasis?
61. The cause of neuronal degeneration in Alzheimer's disease
62. Camptothecin and taxol: Discovery to clinic - Thirteenth Bruce F. Cain memorial award lecture
63. Microtubule-interfering agents activate c-Jun N-terminal kinase/stress-activated protein kinase through both Ras and apoptosis signal-regulating kinase pathways
64. Microtubule dysfunction induced by paclitaxel initiates apoptosis through both c-Jun N-terminal kinase (JNK)-dependent and -independent pathways in ovarian cancer cells
65. Phosphorylation of c-Jun is necessary for apoptosis induced by survival signal withdrawal in cerebellar granule neurons
66. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis
67. Calcium influx via the NMDA receptor induces immediate early gene transcription by a MAP kinase/ERK-dependent mechanism
68. Dynamic regulation of c-Jun N-terminal kinase activity in mouse brain by environmental stimuli
69. BCL-2 is phosphorylated and inactivated by an ASK1/Jun N-terminal protein kinase pathway normally activated at G(2)/M
70. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
71. Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor
72. The stress-activated protein kinase pathway mediates cell death following injury induced by cis-platinum, UV irradiation or heat