Redox modifier genes in amyotrophic lateral sclerosis in mice. - Wikidata - awgldk - TriplyDB

Redox modifier genes in amyotrophic lateral sclerosis in mice.

Redox modifier genes in amyotrophic lateral sclerosis in mice.

http://www.wikidata.org/entity/Q35987578

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SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model Redox control of microglial function: molecular mechanisms and functional significance Rho family GTPases: key players in neuronal development, neuronal survival, and neurodegeneration HCV Tumor Promoting Effect Is Dependent on Host Genetic Background Mitochondrial Cu,Zn-superoxide dismutase mediates pulmonary fibrosis by augmenting H2O2 generation NADPH oxidase 1-mediated oxidative stress leads to dopamine neuron death in Parkinson's disease Adaptive immune neuroprotection in G93A-SOD1 amyotrophic lateral sclerosis mice.New insights on NOX enzymes in the central nervous system.Redox modifier genes and pathways in amyotrophic lateral sclerosis.Spinal cord pathology is ameliorated by P2X7 antagonism in a SOD1-mutant mouse model of amyotrophic lateral sclerosis Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis.Targeting NOX enzymes in the central nervous system: therapeutic opportunities.Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice The nicotinamide adenine dinucleotide phosphate oxidase (NOX) homologues NOX1 and NOX2/gp91(phox) mediate hepatic fibrosis in mice Signaling events in axons and/or dendrites render motor neurons vulnerable to mutant superoxide dismutase toxicity Endogenous regulatory T lymphocytes ameliorate amyotrophic lateral sclerosis in mice and correlate with disease progression in patients with amyotrophic lateral sclerosis.The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease.Alsin and SOD1(G93A) proteins regulate endosomal reactive oxygen species production by glial cells and proinflammatory pathways responsible for neurotoxicity Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling NADPH oxidase mediated oxidative stress in hepatic fibrogenesis NOX2 As a Target for Drug Development: Indications, Possible Complications, and Progress.NADPH oxidases: novel therapeutic targets for neurodegenerative diseases Revisiting oxidative damage in ALS: microglia, Nox, and mutant SOD1 Motor neuron-immune interactions: the vicious circle of ALS.Roles of vitamin D in amyotrophic lateral sclerosis: possible genetic and cellular signaling mechanisms.Different regulation of wild-type and mutant Cu,Zn superoxide dismutase localization in mammalian mitochondria.T lymphocytes potentiate endogenous neuroprotective inflammation in a mouse model of ALS.Diapocynin and apocynin administration fails to significantly extend survival in G93A SOD1 ALS mice.Phosphorylation of Nox1 regulates association with NoxA1 activation domain.Therapeutic AAV9-mediated suppression of mutant SOD1 slows disease progression and extends survival in models of inherited ALS The prostaglandin E2 EP2 receptor accelerates disease progression and inflammation in a model of amyotrophic lateral sclerosis.Extracellular mutant SOD1 induces microglial-mediated motoneuron injury.Regulatory T lymphocytes from ALS mice suppress microglia and effector T lymphocytes through different cytokine-mediated mechanisms.Abnormal intracellular calcium signaling and SNARE-dependent exocytosis contributes to SOD1G93A astrocyte-mediated toxicity in amyotrophic lateral sclerosis.Astrocytes expressing mutant SOD1 and TDP43 trigger motoneuron death that is mediated via sodium channels and nitroxidative stress.NADPH oxidase in brain injury and neurodegenerative disorders SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments.Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis.The neuroprotective effects of apocynin.Physiological roles of NOX/NADPH oxidase, the superoxide-generating enzyme.

P2860

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P2860

Redox modifier genes in amyotrophic lateral sclerosis in mice.

http://www.wikidata.org/entity/Q35987578

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice.

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Redox modifier genes in amyotrophic lateral sclerosis in mice

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P2093

Aislinn J Williams

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Henry Paulson

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Jennifer J Marden

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Kathryn Nelson

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Maged M Harraz

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Meihui Luo

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P2860

Nox1-dependent reactive oxygen generation is regulated by Rac1

Involvement of Rac1 in activation of multicomponent Nox1- and Nox3-based NADPH oxidases

Mouse model of X-linked chronic granulomatous disease, an inherited defect in phagocyte superoxide production

Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

Decreased blood pressure in NOX1-deficient mice

NOX enzymes and the biology of reactive oxygen

Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

Unraveling the mechanisms involved in motor neuron degeneration in ALS

Onset and progression in inherited ALS determined by motor neurons and microglia

RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse model.

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amyotrophic lateral sclerosis

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