Muscle mitochondrial uncoupling dismantles neuromuscular junction and triggers distal degeneration of motor neurons. - Wikidata - awgldk - TriplyDB

Muscle mitochondrial uncoupling dismantles neuromuscular junction and triggers distal degeneration of motor neurons.

Muscle mitochondrial uncoupling dismantles neuromuscular junction and triggers distal degeneration of motor neurons.

http://www.wikidata.org/entity/Q37165781

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Sperm and oocyte communication mechanisms controlling C. elegans fertility ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium Triad The Neuromuscular Junction: Aging at the Crossroad between Nerves and Muscle The Onecut transcription factor HNF-6 regulates in motor neurons the formation of the neuromuscular junctions Skeletal Muscle Satellite Cells, Mitochondria, and MicroRNAs: Their Involvement in the Pathogenesis of ALS The complex molecular biology of amyotrophic lateral sclerosis (ALS)ALS as a distal axonopathy: molecular mechanisms affecting neuromuscular junction stability in the presymptomatic stages of the disease Partial loss of TDP-43 function causes phenotypes of amyotrophic lateral sclerosis.Motor neuron intrinsic and extrinsic mechanisms contribute to the pathogenesis of FUS-associated amyotrophic lateral sclerosis.Distinct changes in synaptic protein composition at neuromuscular junctions of extraocular muscles versus limb muscles of ALS donors.Downregulation of genes with a function in axon outgrowth and synapse formation in motor neurones of the VEGFdelta/delta mouse model of amyotrophic lateral sclerosis.Androgen receptors in muscle fibers induce rapid loss of force but not mass: implications for spinal bulbar muscular atrophy.Blood biomarkers for amyotrophic lateral sclerosis: myth or reality?Role of mitochondria in mutant SOD1 linked amyotrophic lateral sclerosis Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).Genetically altering organismal metabolism by leptin-deficiency benefits a mouse model of amyotrophic lateral sclerosis Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration Analysis of neurotrophic factors in limb and extraocular muscles of mouse model of amyotrophic lateral sclerosis Smads as muscle biomarkers in amyotrophic lateral sclerosis Mitochondrial network genes in the skeletal muscle of amyotrophic lateral sclerosis patients Perturbations in intracellular Ca2+ handling in skeletal muscle in the G93A*SOD1 mouse model of amyotrophic lateral sclerosis.Systemic down-regulation of delta-9 desaturase promotes muscle oxidative metabolism and accelerates muscle function recovery following nerve injury.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.Motor neuron trophic factors: therapeutic use in ALS?Thermogenic ability of uncoupling protein 1 in beige adipocytes in mice.Genotype-property patient-phenotype relations suggest that proteome exhaustion can cause amyotrophic lateral sclerosis.Secreted VAPB/ALS8 major sperm protein domains modulate mitochondrial localization and morphology via growth cone guidance receptors.A metabolic switch toward lipid use in glycolytic muscle is an early pathologic event in a mouse model of amyotrophic lateral sclerosis Measuring Neuromuscular Junction Functionality in the SOD1(G93A) Animal Model of Amyotrophic Lateral Sclerosis.Autophagy impairment in muscle induces neuromuscular junction degeneration and precocious aging.Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Neurogenic and myogenic contributions to hereditary motor neuron disease.Molecular signatures of amyotrophic lateral sclerosis disease progression in hind and forelimb muscles of an SOD1(G93A) mouse model Dietary restriction attenuates age-associated muscle atrophy by lowering oxidative stress in mice even in complete absence of CuZnSOD.Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.Functional classification of skeletal muscle networks. II. Applications to pathophysiology.Complement activation at the motor end-plates in amyotrophic lateral sclerosis.Skeletal muscle in motor neuron diseases: therapeutic target and delivery route for potential treatments.Enhanced uncoupling of the mitochondrial respiratory chain as a potential source for amyotrophic lateral sclerosis

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Muscle mitochondrial uncoupling dismantles neuromuscular junction and triggers distal degeneration of motor neurons.

http://www.wikidata.org/entity/Q37165781

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 30 April 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

@en

Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

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type

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Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

@en

Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

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prefLabel

Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

@en

Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

@nl

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JOURNAL.PONE.0005390

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Muscle mitochondrial uncouplin ...... degeneration of motor neurons.

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Andoni Echaniz-Laguna

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Benoit Halter

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Caroline Huze

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Frédérique Rene

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Hugues Oudart

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Jean-Philippe Loeffler

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Jose-Luis Gonzalez de Aguilar

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Judith Eschbach

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Laurent Schaeffer

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Luc Dupuis

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P2860

Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy

Nogo provides a molecular marker for diagnosis of amyotrophic lateral sclerosis

ALS: a disease of motor neurons and their nonneuronal neighbors

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

No benefit of dietary restriction on disease onset or progression in amyotrophic lateral sclerosis Cu/Zn-superoxide dismutase mutant mice.

Energy intake and amyotrophic lateral sclerosis.

Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis

Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis

Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis.

Congenital muscular dystrophy: molecular and cellular aspects.

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e5390

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scholarly article

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10.1371/JOURNAL.PONE.0005390

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4

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4

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Frederic Bouillaud

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2009-04-30T00:00:00Z

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24379182

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19404401

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2671839

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