HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy - Wikidata - awgldk - TriplyDB

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

http://www.wikidata.org/entity/Q27311425

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Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice.Regulation of class IIa HDAC activities: it is not only matter of subcellular localization SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice.Fast-to-Slow Transition of Skeletal Muscle Contractile Function and Corresponding Changes in Myosin Heavy and Light Chain Formation in the R6/2 Mouse Model of Huntington's Disease Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the HdhQ150/Q150 Mouse Model of Huntington's Disease.Frequency of nuclear mutant huntingtin inclusion formation in neurons and glia is cell-type-specific.Progressive Cl- channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington's mice.Transcriptional Signature of an Altered Purine Metabolism in the Skeletal Muscle of a Huntington's Disease Mouse Model Huntington's disease is a multi-system disorder.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.A shared mechanism of muscle wasting in cancer and Huntington's disease.Changes in cardiac nucleotide metabolism in Huntington's disease.Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.Neuro-Cardio Mechanisms in Huntington's Disease and Other Neurodegenerative Disorders.

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

http://www.wikidata.org/entity/Q27311425

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2015 թուականի Մարտին հրատարակուած գիտական յօդուած

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2015 թվականի մարտին հրատարակված գիտական հոդված

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2015年の論文

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

@en

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

@nl

prefLabel

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

@ast

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

@en

HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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JOURNAL.PGEN.1005021

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HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy

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Cleo J L M Smeets

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Izabela Piotrowska

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James R T Dick

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Linda Greensmith

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Marie K Bondulich

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Marta Toczek

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Mhoriam Ahmed

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Nelly Jolinon

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Sophie A Franklin

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Thomas Muller

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P2860

VITO-1 is an essential cofactor of TEF1-dependent muscle-specific gene regulation

Transcription enhancer factor 1 binds multiple muscle MEF2 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions

SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntington's disease

HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration

The hunt for huntingtin function: interaction partners tell many different stories

Plasma neurofilament heavy chain levels correlate to markers of late stage disease progression and treatment response in SOD1(G93A) mice that model ALS

Increased apoptosis and early embryonic lethality in mice nullizygous for the Huntington's disease gene homologue

Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype

Neurological abnormalities in a knock-in mouse model of Huntington's disease

HDAC4 does not act as a protein deacetylase in the postnatal murine brain in vivo

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e1005021

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scholarly article

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2654701

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10.1371/JOURNAL.PGEN.1005021

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3

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11

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Michal Mielcarek

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2015-03-01T00:00:00Z

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273258049

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25748626

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4352047

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