Mitochondrial disappearance from cells: A clue to the role of autophagy in programmed cell death and disease?

Biochimie

Volumn 84, Issue 2-3, 2002, Pages 233-240

  Tolkovsky, Aviva M ^a   Xue, Luzheng ^a   Fletcher, Graham C ^a   Borutaite, Vilma ^a  

^a Department of Biochemistry ^*  (United Kingdom)

Author keywords

Apoptosis; Autophagy; Caspases; Cell death; Mitochondria; Neurons

Indexed keywords

3 METHYLADENINE; BAFILOMYCIN A1; BENZYLOXYCARBONYLVALYLALANYLASPARTYL FLUOROMETHYL KETONE; CALCINEURIN INHIBITOR; CASPASE INHIBITOR; CYCLOSPORIN A; CYTARABINE; ETOPOSIDE; MITOCHONDRIAL DNA; NERVE GROWTH FACTOR; PROTEIN BCL 2; STAUROSPORINE; TACROLIMUS;

ADOPTIVE IMMUNOTHERAPY; APOPTOSIS; AUTOPHAGY; CELL GROWTH; CELL LINE; CELL ORGANELLE; CELL STRAIN 3T3; CELL STRUCTURE; CHO CELL; DRUG EFFECT; DRUG TARGETING; GENE INDUCTION; GENE OVEREXPRESSION; HELA CELL; HOUSEKEEPING GENE; HUMAN; INSECT; MAMMAL CELL; MITOCHONDRION; MOLTING; NERVOUS SYSTEM; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PHYSICAL DISEASE; PROTEIN DEGRADATION; REVIEW; SIGNAL TRANSDUCTION; SYMPATHETIC NERVE CELL;

HEXAPODA; MAMMALIA;

EID: 0036479052     PISSN: 03009084     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0300-9084(02)01371-8     Document Type: Article

References (67)

1. The turnover of mitochondria in a variety of tissues of young adult and aged rats
2. Programmed cell death. Cytochemical evidence for lysosomes during the normal breakdown of the intersegmental muscles
3. Changes of mitochondrial mass in the hemopoietic stem cell line FDCP-mix after treatment with etoposide: A correlative study by multiparameter flow cytometry and confocal and electron microscopy
4. Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death
5. FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex
6. Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death
7. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
8. Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death
9. Caspase activity sows the seeds of neuronal death
10. Cortical cell death induced by IL-1 is mediated via actions in the hypothalamus of the rat
11. Stroke treatment enters the Fas lane
12. Inhibition of Ced-3/ICE-related proteases does not prevent cell death induced by oncogenes, DNA damage, or the Bcl-2 homologue Bak
13. Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization
14. The point of no return: Mitochondria, caspases, and the commitment to cell death
15. Energy requirement for caspase activation and neuronal cell death
16. Death commitment point is advanced by axotomy in sympathetic neurons
17. Mitochondria are selectively eliminated from eukaryotic cells after blockade of caspases during apoptosis
18. Apoptosis inducing factor (AIF): A phylogenetically old, caspase-independent effector of cell death
19. Endonuclease G is an apoptotic DNase when released from mitochondria
20. Autophagy is activated by apoptotic signalling in sympathetic neurons: An alternative mechanism of death execution
21. Autophagy as a regulated pathway of cellular degradation
22. Molecular dissection of autophagy: Two ubiquitin-like systems
23. The autophagosomal-lysosomal compartment in programmed cell death
24. Temporal analysis of events associated with programmed cell death (apoptosis) of sympathetic neurons deprived of nerve growth factor
25. Inhibition by insulin of the formation of autophagic vacuoles in rat liver. A morphometric approach to the kinetics of intracellular degradation by autophagy
26. A role for MAPK/ERK in sympathetic neuron survival: Protection against a p53-dependent, JNK-independent induction of apoptosis by cytosine arabinoside
27. The Ras/phosphatidylinositol 3-kinase and Ras/ERK pathways function as independent survival modules each of which inhibits a distinct apoptotic signaling pathway in sympathetic neurons
28. DNA inclusions within autolytic cytoplasmic vacuoles of hemopoietic stem cell line FDCP-Mix
29. Origins of hydrogenosomes and mitochondria: Evolution and organelle biogenesis
30. Mechanisms of mitochondrial DNA escape to the nucleus in the yeast Saccharomyces cerevisiae
31. 3-Methyladenine: Specific inhibitor of autophagic/lysosomal protein degradation in isolated rat hepatocytes
32. Inhibition of autophagy abrogates tumour necrosis factor alpha induced apoptosis in human T-lymphoblastic leukaemic cells
33. 3-Methyladenine, an inhibitor of autophagy, has multiple effects on metabolism
34. Distinct classes of phosphatidylinositol 3'-kinases are involved in signaling pathways that control macroautophagy in HT-29 cells
35. JNK and p38 stresskinases-degenerative effectors of signal- transduction-cascades in the nervous system
36. Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway
37. Inhibition of JNK by overexpression of the JNL binding domain of JIP-1 prevents apoptosis in sympathetic neurons
38. A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c
39. Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction
40. Functional F1-ATPase essential in maintaining growth and membrane potential of human mitochondrial DNA-depleted rho degrees cells
41. Quantitation and origin of the mitochondrial membrane potential in human cells lacking mitochondrial DNA
42. Ethidium bromide-induced inhibition of mitochondrial gene transcription suppresses glucose-stimulated insulin release in the mouse pancreatic beta-cell line beta HC9
43. Targeted disruption of mouse conventional kinesin heavy chain, kif5B, results in abnormal perinuclear clustering of mitochondria
44. Bcl-2 down-regulation causes autophagy in a caspase-independent manner in human leukemic HL60 cells
45. Control of mitochondrial morphology by a human mitofusin
46. Dynamin-related protein drp1 is required for mitochondrial division in mammalian cells
47. Bax and Bak coalesce into novel mitochondria-associated clusters during apoptosis
48. Ultrastructural study of the normal degeneration of the intersegmental muscles of Anthereae polyphemus and Manduca sexta (Insecta, Lepidoptera) with particular reference of cellular autophagy
49. The mitochondrial permeability transition in cell death: A common mechanism in necrosis, apoptosis and autophagy
50. The mitochondrial permeability transition initiates autophagy in rat hepatocytes
51. The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event
52. Apg14p and Apg6/Vps30p form a protein complex essential for autophagy in the yeast, Saccharomyces cerevisiae
53. Protection against fatal Sindbis virus encephalitis by beclin, a novel Bcl-2-interacting protein
54. Induction of autophagy and inhibition of tumorigenesis by beclin 1
55. Active cell death induced by the anti-estrogens tamoxifen and ICI 164 384 in human mammary carcinoma cells (MCF-7) in culture: The role of autophagy
56. Beclin-phosphatidylinositol 3-kinase complex functions at the trans-Golgi network
57. Autophagy in embryonic erythroid cells: Its role in maturation
58. Caspase activation is required for terminal erythroid differentiation
59. Turnover of F1F0-ATP synthase subunit 9 and other proteolipids in normal and Batten disease fibroblasts
60. Biochemistry of neuronal ceroid lipofuscinoses
61. Mitochondrial abnormalities in Alzheimer's disease
62. Control of neuronal size homeostasis by trophic factor-mediated coupling of protein degradation to protein synthesis
63. ER stress response: Getting the UPR hand on misfolded proteins
64. Inter-mitochondrial complementation: Mitochondria-specific system preventing mice from expression of disease phenotypes by mutant mtDNA
65. Human cells are protected from mitochondrial dysfunction by complementation of DNA products in fused mitochondria
66. Injection of mitochondria into human cells leads to a rapid replacement of the endogenous mitochondrial DNA