Amyotrophic Lateral Sclerosis, New England Journal of Medicine, vol.344, issue.22, pp.1688-1700, 2001. ,
DOI : 10.1056/NEJM200105313442207
Apoptosis in amyotrophic lateral sclerosis: a review of the evidence, Neuropathology and Applied Neurobiology, vol.90, issue.405, pp.257-274, 2001. ,
DOI : 10.1038/32681
Widespread loss of neuronal populations in the spinal ventral horn in sporadic motor neuron disease. A morphometric study, Journal of the Neurological Sciences, vol.244, issue.1-2, pp.244-285, 2006. ,
DOI : 10.1016/j.jns.2005.12.003
Cortical selective vulnerability in motor neuron disease: a morphometric study, Brain, vol.127, issue.6, pp.1237-1251, 2004. ,
DOI : 10.1093/brain/awh132
Amyotrophic lateral sclerosis: from current developments in the laboratory to clinical implications, Antiox. Redox Sig, pp.405-443, 2008. ,
TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis, Nat. Genet, vol.40, pp.572-574, 2008. ,
Mitochondriopathy in Parkinson Disease and Amyotrophic Lateral Sclerosis, Journal of Neuropathology and Experimental Neurology, vol.65, issue.12, pp.1103-1110, 2006. ,
DOI : 10.1097/01.jnen.0000248541.05552.c4
Genetics of sporadic amyotrophic lateral sclerosis, Human Molecular Genetics, vol.16, issue.R2, pp.233-242, 2007. ,
DOI : 10.1093/hmg/ddm215
Molecular mechanisms of cerebral ischemia-induced neuronal death, Internatl. Rev. Cytology, vol.211, pp.93-148, 2002. ,
DOI : 10.1016/S0074-7696(02)21011-6
The mitochondrion as, Janus Bifrons Biochemistry (Moscow), pp.72-1115, 2007. ,
Mitochondrial function and dysfunction in the cell: its relevance to aging and aging-related disease, The International Journal of Biochemistry & Cell Biology, vol.34, issue.11, pp.1372-1381, 2002. ,
DOI : 10.1016/S1357-2725(02)00077-8
Neurodegeneration in Excitotoxicity, Global Cerebral Ischemia, and Target Deprivation: A Perspective on the Contributions of Apoptosis and Necrosis, Brain Research Bulletin, vol.46, issue.4, pp.46-281, 1998. ,
DOI : 10.1016/S0361-9230(98)00024-0
Apoptosis in perinatal hypoxic???ischemic brain injury: How important is it and should it be inhibited?, Brain Research Reviews, vol.50, issue.2, pp.50-244, 2005. ,
DOI : 10.1016/j.brainresrev.2005.07.003
Failure to complete apoptosis following neonatal hypoxia???ischemia manifests as ???continuum??? phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrain, Neuroscience, vol.149, issue.4, pp.822-833, 2007. ,
DOI : 10.1016/j.neuroscience.2007.06.060
Ultrastructural change of synapses of Betz cells in patients with amyotrophic lateral sclerosis, Neuroscience Letters, vol.268, issue.1, pp.29-32, 1999. ,
DOI : 10.1016/S0304-3940(99)00374-2
Mitochondrial involvement in amyotrophic lateral sclerosis, Neurochemistry International, vol.40, issue.6, pp.543-551, 2002. ,
DOI : 10.1016/S0197-0186(01)00125-5
Cytochrome c oxidase subunit I microdeletion in a paitent with motor neuron disease, Ann. Neurol, pp.43110-116, 1998. ,
Motor neuron disease in a patient with a mitochondrial tRNAIle mutation, Ann. Neurol, pp.59-570, 2006. ,
Mosaicism for a specific somatic mitochondrial DNA mutation in adult human brain, Nature Genetics, vol.290, issue.4, pp.318-323, 1992. ,
DOI : 10.1016/0197-4580(87)90127-8
Mitochondrial DNA deletions in human brain: regional variability and increase with advanced age, Nature Genetics, vol.640, issue.4, pp.324-329, 1992. ,
DOI : 10.1001/jama.262.18.2551
Single-cell analysis of mtDNA deletion levels in sporadic amyotrophic lateral sclerosis, NeuroReport, vol.15, issue.6, pp.939-943, 2004. ,
DOI : 10.1097/00001756-200404290-00002
Amyotrophic lateral sclerosis linked to a novel SOD1 mutation with muscle mitochondrial dysfunction, Journal of the Neurological Sciences, vol.276, issue.1-2, pp.276-170, 2009. ,
DOI : 10.1016/j.jns.2008.09.030
Mitochondrial oversight of cellular Ca2+ signaling, Current Opinion in Neurobiology, vol.8, issue.3, pp.398-404, 1998. ,
DOI : 10.1016/S0959-4388(98)80067-6
Ultrastructural evidence for altered calcium in motor nerve terminals in amyotrophc lateral sclerosis, Annals of Neurology, vol.148, issue.2, pp.203-216, 1996. ,
DOI : 10.1002/ana.410390210
The mitochondrial permeability transition, Biochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, vol.1241, issue.2, pp.139-176, 1995. ,
DOI : 10.1016/0304-4157(95)00003-A
Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate, Science, vol.164, issue.3880, pp.366-368, 1969. ,
DOI : 10.1126/science.164.3880.719
Neurodegeneration: Cellular defences destroyed, Nature, vol.15, issue.7027, pp.696-698, 2005. ,
DOI : 10.1038/sj.cdd.4401042
Synaptic mitochondria are more susceptible to Ca 2+ overload than nonsynaptic mitochondria, J. Biol. Chem, pp.281-11658, 2006. ,
Decreased Glutamate Transport by the Brain and Spinal Cord in Amyotrophic Lateral Sclerosis, New England Journal of Medicine, vol.326, issue.22, pp.1464-1468, 1992. ,
DOI : 10.1056/NEJM199205283262204
Selective loss of glial glutamate transporter GLT-1 in amyotrophic lateral sclerosis, Annals of Neurology, vol.20, issue.1, pp.38-73, 1995. ,
DOI : 10.1002/ana.410380114
Quantitative assessment of AMPA receptor mRNA in human spinal motor neurons isolated by laser capture microdissection, NeuroReport, vol.13, issue.14, pp.1753-1757, 2002. ,
DOI : 10.1097/00001756-200210070-00012
Deficient RNA editing of GluR2 and neuronal death in amyotropic lateral sclerosis, Journal of Molecular Medicine, vol.14, issue.2, pp.110-120, 2005. ,
DOI : 10.1007/s00109-004-0599-z
Mitochondrial trafficking and motphology in healthy and injured neurons, Prog, Brain Res, vol.80, pp.241-268, 2006. ,
Calcium-induced generation of reactive oxygen species in brain mitochondria is mediated by permeability transition, Free Radic, Biol. Med, pp.45-284, 2008. ,
levels in brainstem motoneurones from mouse, The Journal of Physiology, vol.80, issue.1, pp.45-59, 2004. ,
DOI : 10.1113/jphysiol.2003.053900
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine, Annual Review of Genetics, vol.39, issue.1, pp.39-359, 2005. ,
DOI : 10.1146/annurev.genet.39.110304.095751
Superoxide Radical and Superoxide Dismutases, Annual Review of Biochemistry, vol.64, issue.1, pp.97-112, 1995. ,
DOI : 10.1146/annurev.bi.64.070195.000525
DNA damage profiling in motor neurons: a single-cell analysis by comet assay, Neurochem. Res, vol.27, pp.1089-1100, 2002. ,
Characterization and function of mitochondrial nitric-oxide synthase, Free Radic, Biol. Med, vol.34, pp.397-408, 2003. ,
and mitochondria, Biochemical Society Symposium, vol.66, pp.17-25, 1999. ,
DOI : 10.1042/bss0660017
Oxidatively modified protein in aging and disease. Free Radic, Biol. Med, vol.32, pp.797-803, 2002. ,
Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis, Journal of Neurochemistry, vol.69, issue.5, pp.69-2064, 1997. ,
DOI : 10.1046/j.1471-4159.1997.69052064.x
Induction of nitrotyrosine-like immunoreactivity in the lower motor neuron of amyotrophic lateral sclerosis, Neuroscience Letters, vol.199, issue.2, pp.199-152, 1995. ,
DOI : 10.1016/0304-3940(95)12039-7
Increased 3-nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis, Annals of Neurology, vol.22, issue.4, pp.42-644, 1997. ,
DOI : 10.1002/ana.410420416
iNOS and nitrotyrosine immunoreactivity in amyotrophic lateral sclerosis, Neuroscience Letters, vol.291, issue.1, pp.44-48, 2000. ,
DOI : 10.1016/S0304-3940(00)01370-7
Metabolic Dysfunction in Familial, but Not Sporadic, Amyotrophic Lateral Sclerosis, Journal of Neurochemistry, vol.71, issue.1, pp.71-281, 1998. ,
DOI : 10.1046/j.1471-4159.1998.71010281.x
Mitochondrial enzyme activity in amyotrophic lateral sclerosis: Implications for the role of mitochondria in neuronal cell death, Annals of Neurology, vol.277, issue.5, pp.46-787, 1999. ,
DOI : 10.1002/1531-8249(199911)46:5<787::AID-ANA17>3.0.CO;2-8
Mitochondrial DNA abnormalities in skeletal muscle of patients with sporadic amyotrophic lateral sclerosis, Brain, vol.123, issue.7, pp.1339-1348, 2000. ,
DOI : 10.1093/brain/123.7.1339
Activities of mitochondrial complexes correlate with nNOS amount in muscle from ALS patients, Neuropathology and Applied Neurobiology, vol.14, issue.2, pp.33-204, 2007. ,
DOI : 10.1006/bbrc.1995.1824
Muscular mitochondrial function in amyotrophic lateral sclerosis is progressively altered as the desiese develops; a temporal study in man, Exp. Neurol. Exp. Neurol, pp.198-223, 2006. ,
Visualization of defective mitochondrial function in skeletal muscle fibers of patients with sporadic amyotrophic lateral sclerosis, Journal of the Neurological Sciences, vol.169, issue.1-2, pp.169-133 ,
DOI : 10.1016/S0022-510X(99)00236-1
On the origin, evolution, and nature of programmed cell death: a timeline of four billion years, Cell Death and Differentiation, vol.9, issue.4, pp.367-393, 2002. ,
DOI : 10.1038/sj.cdd.4400950
BCL-2 GENE FAMILY IN THE NERVOUS SYSTEM, Annual Review of Neuroscience, vol.20, issue.1, pp.245-267, 1997. ,
DOI : 10.1146/annurev.neuro.20.1.245
The bcl2 family: regulators of the cellular life-or-death switch, Nature Reviews Cancer, vol.2, issue.9, pp.647-656, 2002. ,
DOI : 10.1038/nrc883
Mitochondrial effectors in caspase-independent cell death, FEBS Letters, vol.270, issue.1-3, pp.14-20, 2004. ,
DOI : 10.1016/S0014-5793(03)01464-9
URL : https://hal.archives-ouvertes.fr/pasteur-00193650
Acetylation of the C Terminus of Ku70 by CBP and PCAF Controls Bax-Mediated Apoptosis, Molecular Cell, vol.13, issue.5, pp.627-638, 2004. ,
DOI : 10.1016/S1097-2765(04)00094-2
Neuronal Death in Amyotrophic Lateral Sclerosis Is Apoptosis, Journal of Neuropathology and Experimental Neurology, vol.58, issue.5, pp.459-471, 1999. ,
DOI : 10.1097/00005072-199905000-00005
Opportunities for neuroprotection in ALS using cell dealth mechanism rationales, Drug Discov. Today, vol.1, pp.135-143, 2004. ,
Neuronal cell death in nervous system development, disease, and injury, Intl, J. Mol. Med, vol.4, pp.455-478, 2001. ,
Cell and tissue microdissection in combination with genomic and proteomic profiling, Neuroanatomical Tract-Tracing 3. Molecules, Neurons, and Systems, pp.109-141, 2006. ,
Molecular Regulation of DNA Damage-Induced Apoptosis in Neurons of Cerebral Cortex, Cerebral Cortex, vol.19, issue.6, pp.1273-1293, 2009. ,
DOI : 10.1093/cercor/bhn167
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis, Science, vol.303, issue.5660, pp.1010-1014, 2004. ,
DOI : 10.1126/science.1092734
p53 Is Abnormally Elevated and Active in the CNS of Patients with Amyotrophic Lateral Sclerosis, Neurobiology of Disease, vol.7, issue.6, pp.613-622, 2000. ,
DOI : 10.1006/nbdi.2000.0314
Injury-induced spinal motor neuron apoptosis is preceded by DNA singlestrand breaks and is p53-and Bax-dependent, J. Neurobiol, pp.50-181, 2002. ,
Lessons from models of SOD1-linked familial ALS, Trends in Molecular Medicine, vol.10, issue.8, pp.393-400, 2004. ,
DOI : 10.1016/j.molmed.2004.06.009
Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS, Progress in Neurobiology, vol.85, issue.1, pp.94-134, 2008. ,
DOI : 10.1016/j.pneurobio.2008.01.001
Superoxide dismutase, an enzymic function for erythrocuprein (hemocuprein), J. Biol. Chem, vol.244, pp.6049-6055, 1969. ,
Monomeric Cu,Zn-superoxide Dismutase Is a Common Misfolding Intermediate in the Oxidation Models of Sporadic and Familial Amyotrophic Lateral Sclerosis, Journal of Biological Chemistry, vol.279, issue.15, pp.279-15499, 2004. ,
DOI : 10.1074/jbc.M313295200
Familial ALS-superoxide dismutases associate with mitochondria and shift their redox potentials, Proc. Natl. Sci. USA 103, pp.13860-13865, 2006. ,
DOI : 10.1073/pnas.0605814103
Induction of nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide dismutase, Science, vol.286, pp.2498-2500, 1999. ,
Overexpression of manganese superoxide dismutase attenuates neuronal death in human cells expressing mutant (G37R) Cu/Zn-superoxide dismutase, Journal of Neurochemistry, vol.81, issue.1, pp.81-170, 2002. ,
DOI : 10.1046/j.1471-4159.2002.00812.x
Low levels of ALSlinked Cu/Zn superoxide dismutase increase the production of reactive oxygen species and cause mitochondrial damage and death in motor neuron-like cells, J. Neurol. Sci, issue.205, pp.323-95 ,
in astrocytes induces functional deficits in motoneuron mitochondria, Journal of Neurochemistry, vol.14, issue.Suppl., pp.1271-1283, 2008. ,
DOI : 10.1111/j.1471-4159.2008.05699.x
Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation, Science, vol.264, issue.5166, pp.1772-1775, 1994. ,
DOI : 10.1126/science.8209258
Development of central nervous system pathology in a murine transgenic model of human amyotrophic lateral sclerosis, Am. J. Pathol, pp.145-1271, 1994. ,
The mitochondrial permeability transition pore in motor neurons: Involvement in the pathobiology of ALS mice, Experimental Neurology, vol.218, issue.2, 2009. ,
DOI : 10.1016/j.expneurol.2009.02.015
Motor neuron degeneration in amyotrophoc lateral sclerosis mutant superoxide dismutase-1 transgenic mice: mechanisms of mitochondriopathy and cell death, J. Comp. Neurol, pp.500-520, 2007. ,
Glycinergic Innervation of Motoneurons Is Deficient in Amyotrophic Lateral Sclerosis Mice, The American Journal of Pathology, vol.174, issue.2, pp.574-585, 2009. ,
DOI : 10.2353/ajpath.2009.080557
Early vacuolization and mitochondrial damage in motor neurons of FALS mice are not associated with apoptosis or with changes in cytochrome oxidase histochemical reactivity, Journal of the Neurological Sciences, vol.191, issue.1-2, pp.191-216, 2001. ,
DOI : 10.1016/S0022-510X(01)00627-X
An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria, Neuron, vol.14, issue.6, pp.1105-1116, 1995. ,
DOI : 10.1016/0896-6273(95)90259-7
Massive mitochondrial degeneration in motor neurons triggers the onset of amyotrophic lateral sclerosis in mice expressing a mutant SOD1, J. Neurosci, vol.18, pp.3241-50, 1998. ,
CuZn superoxide dismutase (SOD1) accumulates in vacuolated mitochondria in transgenic mice expressing amyotrophic lateral sclerosis-linked SOD1 mutations, Acta Neuropathol, vol.102, pp.293-305, 2001. ,
Zn Superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS, J. Neurosci, vol.22, pp.1-6, 2002. ,
ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes, BMC Neuroscience, vol.4, issue.1, p.16, 2003. ,
DOI : 10.1186/1471-2202-4-16
Swelling and vacuolation or mitochondria in transgenic SOD1-ALS mice: a consequence of supranormal SOD1 expression? Mitochondrion, pp.48-49, 2006. ,
Ultrastructural study of mitochondria in the spinal cord of transgenic mice with a G93A mutant SOD1 gene, Acta Neuropathologica, vol.107, issue.5, pp.461-474, 2004. ,
DOI : 10.1007/s00401-004-0837-z
Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase, Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase, pp.1047-1051, 1993. ,
DOI : 10.1126/science.8351519
Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity., Proc. Natl. Acad. Sci. USA 91, pp.8292-8296, 1994. ,
DOI : 10.1073/pnas.91.17.8292
A gain-offunction of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant: an enhancement of free radical formation due to a decrease in K m for hydrogen peroxide, Proc. Natl. Acad. Sci. USA 93, pp.5709-5714, 1996. ,
Oxidized/misfolded superoxide dismutase-1: the cause of all amyotrophic lateral sclerosis?, Annals of Neurology, vol.280, issue.6, pp.62-553, 2007. ,
DOI : 10.1002/ana.21319
Wild-type superoxide dismutase acquires binding and toxic properties of ALS-linked mutant forms through oxidation, Journal of Neurochemistry, vol.56, issue.1, pp.170-178, 2007. ,
DOI : 10.1073/pnas.87.13.5006
Mutant Cu,Zn superoxide dismutases and familial amyotrophic lateral sclerosis: evaluation of oxidative hypotheses, Free Radical Biology and Medicine, vol.34, issue.11, pp.1383-1389, 2003. ,
DOI : 10.1016/S0891-5849(03)00153-9
Nitric Oxide and Peroxynitrite in Health and Disease, Physiological Reviews, vol.87, issue.1, pp.315-424, 2007. ,
DOI : 10.1152/physrev.00029.2006
Protein oxidative damage in a transgenic mouse medel of familial amyotrophic lateral sclerosis, J. Neurochem, pp.71-2041, 1998. ,
Redox proteomics analysis of oxidatively modified proteins in G93A-SOD1 transgenic mice-a model of familial amyotrophic lateral sclerosis. Free Radic, Biol. Med, pp.39-435, 2005. ,
Subcellular Distribution of Superoxide Dismutases (SOD) in Rat Liver: Cu,Zn-SOD IN MITOCHONDRIA, Journal of Biological Chemistry, vol.276, issue.42, pp.38388-38393, 2001. ,
DOI : 10.1074/jbc.M105395200
Toxicity of Familial ALS-Linked SOD1 Mutants from Selective Recruitment to Spinal Mitochondria, Neuron, vol.43, issue.1, pp.5-15, 2004. ,
DOI : 10.1016/j.neuron.2004.06.016
Amyotrophic Lateral Sclerosis-Associated SOD1 Mutant Proteins Bind and Aggregate with Bcl-2 in Spinal Cord Mitochondria, Neuron, vol.43, issue.1, pp.19-30, 2004. ,
DOI : 10.1016/j.neuron.2004.06.021
Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondria, Proc. Natl. Acad. Sci. USA 105, pp.4022-4027, 2008. ,
DOI : 10.1073/pnas.0712209105
Deleterious Role of Superoxide Dismutase in the Mitochondrial Intermembrane Space, Journal of Biological Chemistry, vol.283, issue.13, pp.283-8446, 2008. ,
DOI : 10.1074/jbc.M706111200
Mutant Superoxide Dismutase 1 Forms Aggregates in the Brain Mitochondrial Matrix of Amyotrophic Lateral Sclerosis Mice, Journal of Neuroscience, vol.25, issue.10, pp.25-2463, 2005. ,
DOI : 10.1523/JNEUROSCI.4385-04.2005
Mutated Human SOD1 Causes Dysfunction of Oxidative Phosphorylation in Mitochondria of Transgenic Mice, Journal of Biological Chemistry, vol.277, issue.33, pp.277-29626, 2002. ,
DOI : 10.1074/jbc.M203065200
Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content, Human Molecular Genetics, vol.16, issue.22, pp.2720-2728, 2007. ,
DOI : 10.1093/hmg/ddm226
Adult Motor Neuron Apoptosis Is Mediated by Nitric Oxide and Fas Death Receptor Linked by DNA Damage and p53 Activation, Journal of Neuroscience, vol.25, issue.27, pp.25-6449, 2005. ,
DOI : 10.1523/JNEUROSCI.0911-05.2005
Intracellular Calcium Parallels Motoneuron Degeneration in SOD-1 Mutant Mice, Journal of Neuropathology & Experimental Neurology, vol.57, issue.6, pp.571-587, 1998. ,
DOI : 10.1097/00005072-199806000-00005
Cu/Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria and perturbs Ca 2+ homeostasis in SOD1 G93A mice, Mol. Pharmacol, pp.75-478, 2009. ,
Neural mitochondrial Ca 2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice, J. Neurochem, pp.961349-1361, 2006. ,
The ? m depolarization that accompanies mitochondrial Ca 2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals, Proc. Natl. Acad. Sci. USA, 2007. ,
Inducible nitric oxide synthase (iNOS) and nitrotyrosine immunoreactivity in the spinal cords of transgenic mice with mutant SOD1 gene, J. Neuropathol. Exp. Neurol, pp.60-839, 2001. ,
Different Metabolic Properties of Mitochondrial Oxidative Phosphorylation in Different Cell Types - Important Implications for Mitochondrial Cytopathies, Experimental Physiology, vol.88, issue.1, pp.149-154, 2003. ,
DOI : 10.1113/eph8802512
Relationship between configuration, function, and permeability in calcium-treated mitochondria, J. Biol. Chem, pp.251-5069, 1976. ,
The mitochondrial permeability transition pore and its role in cell death, Biochemical Journal, vol.341, issue.2, pp.233-249, 1999. ,
DOI : 10.1042/bj3410233
Mitochondrial intermembrane proteins in cell death, Biochemical and Biophysical Research Communications, vol.304, issue.3, pp.487-497, 2003. ,
DOI : 10.1016/S0006-291X(03)00621-1
The mitochondrial permeability transition from in vitro artifact to disease target, FEBS Journal, vol.14, issue.10, pp.2077-2099, 2006. ,
DOI : 10.1093/hmg/7.13.2135
Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore, Biochimica et Biophysica Acta (BBA) - Bioenergetics, vol.1777, issue.7-8, pp.946-952, 2008. ,
DOI : 10.1016/j.bbabio.2008.03.009
The Voltage-Dependent Anion Channel (VDAC): Function in Intracellular Signalling, Cell Life and Cell Death, Current Pharmaceutical Design, vol.12, issue.18, pp.12-2249, 2006. ,
DOI : 10.2174/138161206777585111
On the Role of VDAC in Apoptosis: Fact and Fiction, Journal of Bioenergetics and Biomembranes, vol.1706, issue.3, pp.129-142, 2005. ,
DOI : 10.1007/s10863-005-6566-8
The Mitochondrial Voltage-dependent Anion Channel (VDAC) as a Therapeutic Target for Initiating Cell Death, Current Medicinal Chemistry, vol.10, issue.16, pp.1527-1533, 2003. ,
DOI : 10.2174/0929867033457214
Human mitochondrial transmembrane metabolite carriers: tissue distribution and its implication for mitochondrial disorders, J. Bioenerg. Biomembr, pp.30-277, 1998. ,
Each mammalian mitochondrial outer membrane porin protein is dispensable: effects on cellular respiration, Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, vol.1452, issue.1, pp.1452-68, 1999. ,
DOI : 10.1016/S0167-4889(99)00120-2
Altered Mitochondrial Sensitivity for ADP and Maintenance of Creatine-stimulated Respiration in Oxidative Striated Muscles from VDAC1-deficient Mice, Journal of Biological Chemistry, vol.276, issue.3, p.276, 1954. ,
DOI : 10.1074/jbc.M006587200
Immotile Sperm and Infertility in Mice Lacking Mitochondrial Voltage-dependent Anion Channel Type 3, Journal of Biological Chemistry, vol.276, issue.42, pp.276-39206, 2001. ,
DOI : 10.1074/jbc.M104724200
VDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis, Science, vol.301, issue.5632, pp.513-517, 2003. ,
DOI : 10.1126/science.1083995
Bax-dependent Regulation of Bak by Voltage-dependent Anion Channel 2, Journal of Biological Chemistry, vol.280, issue.19, pp.19051-19061, 2005. ,
DOI : 10.1074/jbc.M501391200
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death, Nature Cell Biology, vol.336, issue.5, pp.550-555, 2007. ,
DOI : 10.1074/jbc.M313717200
The Adenine Nucleotide Translocase: A Central Component of the Mitochondrial Permeability Transition Pore and Key Player in Cell Death, Current Medicinal Chemistry, vol.10, issue.16, pp.1507-1525, 2003. ,
DOI : 10.2174/0929867033457278
A mouse model for mitochondrial myopathy and cardiomyopathy resulting from a deficiency in the heart/muscle isoform of the adenine nucleotide translocator, Nature Genetics, vol.25, issue.3, pp.16-226, 1997. ,
DOI : 10.1016/S0076-6879(96)64044-0
Differential expression of adenine nucleotide transloactor isoforms in mammalian tissues and during muscle cell differentiation, J. Bio. Chem, vol.267, pp.14592-14597, 1992. ,
Adenine nucleotide translocator isoforms 1 and 2 are differently distrubited in the mitochondrial inner membrane and have distinct affinities to cyclophilin D, Biochem. J, pp.358-349, 2001. ,
The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore, Nature, vol.427, issue.6973, pp.461-465, 2004. ,
DOI : 10.1038/nature02229
A novel adenine nucleotide translocase inhibitor, MT-21, induces cytochrome c release through a mitochondrial permeability transition-independent mechanisms, J. Biol. Chem, pp.277-31243, 2002. ,
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death, Nature, vol.65, issue.7033, pp.658-662, 2005. ,
DOI : 10.1038/sj.gt.3301048
Mitochondria and aging: a role for the permeability transition?, Aging Cell, vol.22, issue.1, pp.3-6, 2004. ,
DOI : 10.1016/0925-4439(95)00021-U
Cyclophilin D as a Drug Target, Current Medicinal Chemistry, vol.10, issue.16, pp.1485-1506, 2003. ,
DOI : 10.2174/0929867033457160
Direct demonstration of a specific interaction between cyclophilin-D and the adenine nucleotide translocase confirms their role in the mitochondrial permeability transition, Biochemical Journal, vol.336, issue.2, pp.336-287, 1998. ,
DOI : 10.1042/bj3360287
Import and processing of heart mitochondrial cyclophilin D, European Journal of Biochemistry, vol.33, issue.2, pp.353-359, 1999. ,
DOI : 10.1126/science.281.5385.2027
Mitochondrial voltage-dependent anion channel, J. Biol. Chem, pp.268-23289, 1993. ,
Subcellular localization of VDAC in mitochondria and ER in the cerebellum, Biochimica et Biophysica Acta (BBA) - Bioenergetics, vol.1657, issue.2-3, pp.105-114, 2004. ,
DOI : 10.1016/j.bbabio.2004.02.009
Voltage-dependent anion channels (VDAC) in the plasma membrane play a critical role in apoptosis in differentiated hippocampal neurons but not in neural stem cells, Cell Cycle, vol.7, issue.20, pp.3225-3234, 2008. ,
DOI : 10.4161/cc.7.20.6831
Subcellular Localization of Human Voltage-dependent Anion Channel Isoforms, Journal of Biological Chemistry, vol.270, issue.23, pp.13998-14006, 1995. ,
DOI : 10.1074/jbc.270.23.13998
Increased adenine nucleotide translocator 1 in reactive astrocytes facilitates glutamate transport, Experimental Neurology, vol.181, issue.2, pp.181149-158, 2003. ,
DOI : 10.1016/S0014-4886(03)00043-8
Cyclophilin D is expressed predominantly in mitochondria of ??-aminobutyric acidergic interneurons, Journal of Neuroscience Research, vol.7, issue.5, pp.1250-1259, 2009. ,
DOI : 10.1002/jnr.21921
High Cyclophilin D Content of Synaptic Mitochondria Results in Increased Vulnerability to Permeability Transition, Journal of Neuroscience, vol.27, issue.28, pp.27-7469, 2007. ,
DOI : 10.1523/JNEUROSCI.0646-07.2007
-isomerase activity associated with the lumen of the endoplasmic reticulum, Biochemical Journal, vol.300, issue.3, pp.865-870, 1994. ,
DOI : 10.1042/bj3000865
URL : https://hal.archives-ouvertes.fr/jpa-00209871
Intrinsic differences in brain and spinal cord mitochondria: Implication for therapeutic interventions, The Journal of Comparative Neurology, vol.22, issue.4, pp.474-524, 2004. ,
DOI : 10.1002/cne.20130
Spinal cord mitochondria display lower calcium retention capacity compared with brain mitochondria without inherent differences in sensitivity to cyclophilin D inhibition, Journal of Neurochemistry, vol.5, issue.5, pp.2066-2076, 2007. ,
DOI : 10.1016/0304-4157(95)00003-A
Mitochondria are morphologically heterogeneous within cells, Journal of Experimental Biology, vol.206, issue.12, 1993. ,
DOI : 10.1242/jeb.00244
Control of mitochondrial shape, Current Opinion in Cell Biology, vol.17, issue.4, pp.384-388, 2005. ,
DOI : 10.1016/j.ceb.2005.06.011
COMPARATIVE STUDIES ON MITOCHONDRIA ISOLATED FROM NEURON-ENRICHED AND GLIA-ENRICHED FRACTIONS OF RABBIT AND BEEF BRAIN, The Journal of Cell Biology, vol.45, issue.2, pp.221-234, 1970. ,
DOI : 10.1083/jcb.45.2.221
Intrathecal cyclosporin prolongs survival of latestage ALS mice, Brain Res, vol.894, pp.27-331, 2001. ,
Life span extension and reduced neuronal death after weekly intraventricular cyclosporin injections in the G93A transgenic mouse model of amyotrophic lateral sclerosis, Journal of Neurosurgery, vol.101, issue.1, pp.128-137, 2004. ,
DOI : 10.3171/jns.2004.101.1.0128
Moraes, An ALS mouse model with a permeable blood-brain barrier benefits from systemic cyclosporine A treatment, J. Neurochem, pp.88-821, 2004. ,
Pruss, identification and characterization of Cholest- 4-en-3-one, oxime (TRO19622), a novel drug candidate for amyotrophic lateral sclerosis, J. Pharmacol. Exp. Ther, pp.322-709, 2007. ,
promotes neonatal motor neuron survival and nerve regeneration in adult rats, Eur. J. Neurosci, pp.5-4864, 2008. ,
Mitochondrial adenine nucleotide translocase is modified oxidatively during aging, Proc. Natl. Acad. Sci. USA 95, pp.12896-12901, 1998. ,
DOI : 10.1073/pnas.95.22.12896
Mass spectrometry-based survey of age-associated protein carboylation in rat brain mitochondria, J. Mass Spectrom, pp.42-1583, 2007. ,
The adenine nucleotide translocator: a target of nitric oxide, peroxynitrite, and 4-hydroxynonenal, Oncogene, vol.20, issue.32, pp.4305-4316, 2001. ,
DOI : 10.1038/sj.onc.1204575
Role of critical thiol groups on the matrix surface of the adenine nucleotide translocase in the mechanism of the mitochondrial permeability transition pore, Biochemical Journal, vol.367, issue.2, pp.367-541, 2002. ,
DOI : 10.1042/bj20011672
Induction of the mitochondrial permeability transition by N-ethylmaleimide depends on secondary oxidation of critical thiol groups. Potentiation by copper-ortho-phenthroline without dimerization of the adenine nucleotide translocase, Biochim. Biophys. Acta, pp.1365-385, 1998. ,
Oxidation of a critical thiol residue of the adenine nucleotide translocator enforces Bcl-2-independent permeability transition pore opening and apoptosis, Oncogene, vol.19, issue.2, pp.307-314, 2000. ,
DOI : 10.1038/sj.onc.1203299
Copper induces permeability transition through its interaction with the adenine nucleotide translocase, Cell Biology International, vol.31, issue.9, pp.31-893, 2007. ,
DOI : 10.1016/j.cellbi.2007.02.003
The permeability transition pore in cell death, Apoptosis, vol.29, issue.257, pp.841-855, 2007. ,
DOI : 10.1007/s10495-007-0747-3
Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease, Nature Medicine, vol.72, issue.10, pp.141097-1105, 2008. ,
DOI : 10.1038/nm.1868
Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, Proc. Natl. Acad. Sci. USA, pp.7558-7563, 2007. ,
DOI : 10.1073/pnas.0702228104
Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia, Proc. Natl. Acad. Sci. USA, pp.12005-12010, 2005. ,
DOI : 10.1073/pnas.0505294102