Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease - Wikidata - awgldk - TriplyDB

Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease

Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease

http://www.wikidata.org/entity/Q27311065

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The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's disease Ups and Downs: Mechanisms of Repeat Instability in the Fragile X-Related Disorders Mitochondrial targeting of XJB-5-131 attenuates or improves pathophysiology in HdhQ150 animals with well-developed disease phenotypes.A selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease mice Putting the Brakes on Huntington Disease in a Mouse Experimental Model Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase.Problems and solutions for the analysis of somatic CAG repeat expansion and their relationship to Huntington's disease toxicity.Oxidized dNTPs and the OGG1 and MUTYH DNA glycosylases combine to induce CAG/CTG repeat instability.DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases Crosstalk between MSH2-MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair.Oxidative Stress and Huntington's Disease: The Good, The Bad, and The Ugly.Huntington Disease as a Neurodevelopmental Disorder and Early Signs of the Disease in Stem Cells.Prodromal spinocerebellar ataxia type 2: Prospects for early interventions and ethical challenges.Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.Precarious maintenance of simple DNA repeats in eukaryotes.Huntingtin is a scaffolding protein in the ATM oxidative DNA damage response complex.Somatic instability of the expanded GAA repeats in Friedreich's ataxia.Minimizing carry-over PCR contamination in expanded CAG/CTG repeat instability applications.Genetic modifiers of Mendelian disease: Huntington's disease and the trinucleotide repeat disorders.The central role of DNA damage and repair in CAG repeat diseases.The Chromatin Remodeler Isw1 Prevents CAG Repeat Expansions During Transcription in Saccharomyces cerevisiae.XJB-5-131-mediated improvement in physiology and behaviour of the R6/2 mouse model of Huntington's disease is age- and sex- dependent.GAA•TTC repeat expansion in human cells is mediated by mismatch repair complex MutLγ and depends upon the endonuclease domain in MLH3 isoform one.Increased nuclear DNA damage precedes mitochondrial dysfunction in peripheral blood mononuclear cells from Huntington's disease patients.Targeting Mitochondrial Oxidative Stress to Mitigate UV-Induced Skin Damage

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Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease

http://www.wikidata.org/entity/Q27311065

description

2015 nî lūn-bûn

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2015 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2015 թվականի օգոստոսին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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Amy Holt

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Bartosz Szczesny

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Cynthia T McMurray

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P2860

Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage

The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington's disease

Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice

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

Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease?

Evidence for a modifier of onset age in Huntington disease linked to the HD gene in 4p16.

Genome-wide significance for a modifier of age at neurological onset in Huntington's disease at 6q23-24: the HD MAPS study.

A genome scan for modifiers of age at onset in Huntington disease: The HD MAPS study.

Tests to assess motor phenotype in mice: a user's guide.

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pathophysiology

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