Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease - Wikidata - awgldk - TriplyDB

Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease

Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease

http://www.wikidata.org/entity/Q35086831

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Mouse models of polyglutamine diseases: review and data table. Part I The N17 domain mitigates nuclear toxicity in a novel zebrafish Huntington's disease model.Reinstating aberrant mTORC1 activity in Huntington's disease mice improves disease phenotypes.Role of oxidative DNA damage in mitochondrial dysfunction and Huntington's disease pathogenesis Clinical classification of cancer cachexia: phenotypic correlates in human skeletal muscle Overexpression of smooth muscle myosin heavy chain leads to activation of the unfolded protein response and autophagic turnover of thick filament-associated proteins in vascular smooth muscle cells Skeletal muscle pathology in Huntington's disease AQP4-dependent water transport plays a functional role in exercise-induced skeletal muscle adaptations Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of duchenne muscular dystrophy Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise Huntington disease skeletal muscle is hyperexcitable owing to chloride and potassium channel dysfunction.Glycolytic-to-oxidative fiber-type switch and mTOR signaling activation are early-onset features of SBMA muscle modified by high-fat diet Ubiquilin-1 overexpression increases the lifespan and delays accumulation of Huntingtin aggregates in the R6/2 mouse model of Huntington's disease.Progressive Cl- channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington's mice.Review: quantifying mitochondrial dysfunction in complex diseases of aging.Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.Mechanisms for fiber-type specificity of skeletal muscle atrophy.Huntingtin promotes mTORC1 signaling in the pathogenesis of Huntington's disease.AMPK-mediated regulation of neuronal metabolism and function in brain diseases.Reduced motivation in the BACHD rat model of Huntington disease is dependent on the choice of food deprivation strategy Chronic 5-Aminoimidazole-4-Carboxamide-1-β-d-Ribofuranoside Treatment Induces Phenotypic Changes in Skeletal Muscle, but Does Not Improve Disease Outcomes in the R6/2 Mouse Model of Huntington's Disease.Ghrelin rescues skeletal muscle catabolic profile in the R6/2 mouse model of Huntington's disease Whole gene expression profile in blood reveals multiple pathways deregulation in R6/2 mouse model.Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.The BACHD Rat Model of Huntington Disease Shows Specific Deficits in a Test Battery of Motor Function.Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.Cardiac mTORC1 Dysregulation Impacts Stress Adaptation and Survival in Huntington's Disease.Dual Therapy with Liraglutide and Ghrelin Promotes Brain and Peripheral Energy Metabolism in the R6/2 Mouse Model of Huntington's Disease.

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Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease

http://www.wikidata.org/entity/Q35086831

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

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AJPENDO.00630.2010

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American Journal of Physiology - Endocrinology and Metabolism

P1476

Molecular characterization of ...... model of Huntington's disease

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Charles H Lang

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Christopher J Lynch

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Deanna Marchionini

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Pengxiang She

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Scot R Kimball

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Thomas C Vary

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Thomas J Jetton

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William C Diaz

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Zhiyou Zhang

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P2860

Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

AMP kinase is required for mitochondrial biogenesis in skeletal muscle in response to chronic energy deprivation.

TSC2 mediates cellular energy response to control cell growth and survival

TOR, a central controller of cell growth.

Sorting, recognition and activation of the misfolded protein degradation pathways through macroautophagy and the proteasome

MURF-1 and MURF-2 target a specific subset of myofibrillar proteins redundantly: towards understanding MURF-dependent muscle ubiquitination

HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS

Ntau-methylhistidine (3-methylhistidine) and muscle protein turnover: an overview

The messenger RNA profiles in liver, hypothalamus, white adipose tissue, and skeletal muscle of female Zucker diabetic fatty rats after topiramate treatment

Identification of ubiquitin ligases required for skeletal muscle atrophy

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E49-61

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scholarly article

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10.1152/AJPENDO.00630.2010

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1

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301

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2011-04-19T00:00:00Z

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51062783

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21505144

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Huntington disease

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3129844

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