Embryonic neuronal death due to neurotrophin and neurotransmitter deprivation occurs independent of Apaf-1

Neuroscience

Volumn 106, Issue 2, 2001, Pages 263-274

  Honarpour, N ^a   Tabuchi, K ^b   Stark, J M ^a   Hammer, R E ^a,b   Sudhof T C ^b   Parada, L F ^b   Wang, X ^a,b   Richardson, J A ^a   Herz, J ^a  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

^b UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

Author keywords

Apoptosis; Caspase; Cell death; Cytochrome c; Mouse; Neuron

Indexed keywords

APOPTOTIC PROTEASE ACTIVATING FACTOR 1; NEUROTRANSMITTER; NEUROTROPHIN; PROTEIN; RECEPTOR SUBUNIT; TYROSINE KINASE RECEPTOR; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL COUNT; CONTROLLED STUDY; EMBRYO; HISTOLOGY; MITOSIS; MOUSE; MOUSE MUTANT; NERVE CELL DIFFERENTIATION; NERVE CELL NECROSIS; NEUROTRANSMITTER RELEASE; NICK END LABELING; NONHUMAN; PRIORITY JOURNAL; PROTEIN ANALYSIS; STEM CELL;

ANIMALS; APOPTOSIS; APOPTOTIC PROTEASE-ACTIVATING FACTOR 1; CASPASES; CELL CYCLE; CELL DIFFERENTIATION; CYTOCHROME C GROUP; GANGLIA, SENSORY; MICE; MICE, KNOCKOUT; MUNC18 PROTEINS; NERVE GROWTH FACTORS; NERVE TISSUE PROTEINS; NERVOUS SYSTEM; NEURONS; NEUROTRANSMITTER AGENTS; PROTEINS; RECEPTOR, TRKA; SIGNAL TRANSDUCTION; STEM CELLS; VESICULAR TRANSPORT PROTEINS;

EID: 0035817727     PISSN: 03064522     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0306-4522(01)00275-5     Document Type: Article

References (51)

1. The Bcl-2 protein family: Arbiters of cell survival
2. Cellular interactions that regulate programmed cell death in the developing vertebrate nervous system
3. Apaf1 (CED-4 homologue) regulated programmed cell death in mammalian development
4. Regressive events in neurogenesis
5. Mitochondrio-nuclear translocation of AIF in apoptosis and necrosis
6. Bax is required for neuronal death after trophic factor deprivation and during development
7. Evidence of a novel event during neuronal death: Development of competence-to-die in response to cytoplasmic cytochrome c
8. Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization
9. Neurodegeneration in Lurcher mice occurs via multiple cell death pathways
10. A conformational switch in syntaxin during exocytosis: Role of munc18
11. Analysis of the mechanism of loss of trophic factor dependence associated with neuronal maturation: A phenotype indistinguishable from Bax deletion
12. Bcl-2 transgene expression can protect neurons against developmental and induced cell death
13. Regulation of exocytosis by cyclin-dependent kinase 5 via phosphorylation of munc18
14. Differential requirement for caspase 9 in apoptotic pathways in vivo
15. Apoptotic protease activating factor-1 (Apaf-1)-independent cell death suppression by Bcl-2
16. nSec-1 (munc-18) interacts with both primed and unprimed syntaxin1A and associates in a dimeric complex on adrenal chromaffin granules
17. Bak BH3 peptides antagonize Bcl-xL function and induce apoptosis through cytochrome c-independent activation of caspases
18. Adult Apaf-1-deficient mice exhibit male infertility
19. Neurotrophins. Keeping track of changing neurotrophic theory
20. Involvement of caspase 3 in apoptotic death of cortical neurons evoked by DNA damage
21. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9
22. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
23. p53 regulates mitochondrial membrane potential through reactive oxygen species and induces cytochrome c-independent apoptosis blocked by Bcl-2
24. Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis
25. Cytochrome c and dATP-dependent formation of Apaf-1/caspase 9 complex initiates an apoptotic protease cascade
26. Loss of brain-derived neurotrophic factor-dependent neural crest-derived sensory neurons in neurotrophin-4 mutant mice
27. The survival of developing neurons: A review of afferent control
28. Bcl-xs and Bax induce different apoptotic pathways in PC12 cells
29. The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues
30. Induction of apoptotic program in cell-free extracts: Requirement for dATP and cytochrome c
31. Overexpression of Bcl-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia
32. Inactivation of Bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development
33. Bax deletion further orders the cell death pathway in cerebellar granule cells and suggests a caspase-independent pathway to cell death
34. Massive cell death of immature hematopoietic cells and neurons in Bcl-x deficient mice
35. Blocking cytochrome c activity within intact neurons inhibits apoptosis
36. Cell death of motoneurons in the chick embryo spinal cord. IX. The loss of motoneurons following removal of afferent inputs
37. Cell death of motoneurons in the chick embryo spinal cord. V. Evidence on the role of cell death and neuromuscular function in the formation of specific peripheral connections
38. The neurotrophic theory and naturally occurring motoneuron death
39. Development of sensory neurons in the absence of NGF/TrkA signaling in vivo
40. Bcl-2 is required for cranial sensory neuron survival at defined stages of embryonic development
41. Amyloid beta-induced neuronal death is Bax-dependent but caspase-independent
42. Severe sensory and sympathetic neuropathies in mice carrying a disrupted Trk/NGF receptor gene
43. Two distinct pathways leading to nuclear apoptosis
44. Bcl-2 family: Life-or-death switch
45. Bax promotes neuronal cell death and is downregulated during the development of the nervous system
46. BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore
47. Synaptic assembly of the brain in the absence of neurotransmitter secretion
48. Homologous recombination for gene replacement in mouse cell lines
49. Apaf1 is required for mitochondrial pathways of apoptosis and brain development
50. BCl-2 mutants with restricted subcellular localization reveal spacially distinct pathways for apoptosis in different cell types
51. Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3