Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
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SPG20 protein spartin associates with cardiolipin via its plant-related senescence domain and regulates mitochondrial Ca2+ homeostasisMitochondrial ubiquitin ligase MITOL ubiquitinates mutant SOD1 and attenuates mutant SOD1-induced reactive oxygen species generationDecreased glutathione accelerates neurological deficit and mitochondrial pathology in familial ALS-linked hSOD1(G93A) mice modelInside out: the role of nucleocytoplasmic transport in ALS and FTLDA comprehensive review of amyotrophic lateral sclerosisSIRT3 regulates progression and development of diseases of aging.Copper delivery to the CNS by CuATSM effectively treats motor neuron disease in SOD(G93A) mice co-expressing the Copper-Chaperone-for-SODMechanisms of oxidative damage in multiple sclerosis and neurodegenerative diseases: therapeutic modulation via fumaric acid estersStructure-function integrity of the adult hippocampus depends on the transcription factor Bcl11b/Ctip2.The legs at odd angles (Loa) mutation in cytoplasmic dynein ameliorates mitochondrial function in SOD1G93A mouse model for motor neuron disease.Protease 3C of hepatitis A virus induces vacuolization of lysosomal/endosomal organelles and caspase-independent cell deathBuilding the power house: recent advances in mitochondrial studies through proteomics and systems biology.Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo.Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.N-acetyl-serotonin protects HepG2 cells from oxidative stress injury induced by hydrogen peroxideNrf2 activation in astrocytes protects against neurodegeneration in mouse models of familial amyotrophic lateral sclerosis.ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.Oxidative stress, mitochondrial damage and neurodegenerative diseasesAbsence of Nrf2 or its selective overexpression in neurons and muscle does not affect survival in ALS-linked mutant hSOD1 mouse models.Functional mitochondrial analysis in acute brain sections from adult rats reveals mitochondrial dysfunction in a rat model of migraine.The effect of SOD1 mutation on cellular bioenergetic profile and viability in response to oxidative stress and influence of mutation-type.Mitochondrial abnormalities and low grade inflammation are present in the skeletal muscle of a minority of patients with amyotrophic lateral sclerosis; an observational myopathology study.The Nrf2-ARE cytoprotective pathway in astrocytes.Motor neuron trophic factors: therapeutic use in ALS?Early gene expression changes in spinal cord from SOD1(G93A) Amyotrophic Lateral Sclerosis animal model.Peroxisome proliferator activator receptor gamma coactivator-1alpha (PGC-1α) improves motor performance and survival in a mouse model of amyotrophic lateral sclerosisReactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signalingOverexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology.An over-oxidized form of superoxide dismutase found in sporadic amyotrophic lateral sclerosis with bulbar onset shares a toxic mechanism with mutant SOD1Slow development of ALS-like spinal cord pathology in mutant valosin-containing protein gene knock-in mice.Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats.Mitochondrial medicine: pharmacological targeting of mitochondria in diseaseAgeing and neuronal vulnerability.Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63.Neuroprotective and Angiogenic Effects of Bone Marrow Transplantation Combined With Granulocyte Colony-Stimulating Factor in a Mouse Model of Amyotrophic Lateral Sclerosis.Isolated cytochrome c oxidase deficiency in G93A SOD1 mice overexpressing CCS proteinMolecular dissection of ALS-associated toxicity of SOD1 in transgenic mice using an exon-fusion approach.Glutamate excitotoxicity and therapeutic targets for amyotrophic lateral sclerosis.SOD1 and DJ-1 converge at Nrf2 pathway: a clue for antioxidant therapeutic potential in neurodegenerationMitochondrial dysfunction in SOD1G93A-bearing astrocytes promotes motor neuron degeneration: prevention by mitochondrial-targeted antioxidants.
P2860
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P2860
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@ast
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@en
type
label
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@ast
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@en
prefLabel
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@ast
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@en
P1433
P1476
Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.
@en
P2093
Giovanni Manfredi
Zuoshang Xu
P356
10.1016/J.MITO.2005.01.002
P577
2005-04-01T00:00:00Z