Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1. - Test2 - elhamkhani - TriplyDB

Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.

Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.

http://www.wikidata.org/entity/Q34021533

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Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington’s Disease The 26S proteasome drives trinucleotide repeat expansions Expansion, mosaicism and interruption: mechanisms of the CAG repeat mutation in spinocerebellar ataxia type 1 The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's disease GFP-based fluorescence assay for CAG repeat instability in cultured human cells Systems biology analysis of Drosophila in vivo screen data elucidates core networks for DNA damage repair in SCA1.Gender and cell-type-specific effects of the transcription-coupled repair protein, ERCC6/CSB, on repeat expansion in a mouse model of the fragile X-related disorders X inactivation plays a major role in the gender bias in somatic expansion in a mouse model of the fragile X-related disorders: implications for the mechanism of repeat expansion.Correlation of inter-locus polyglutamine toxicity with CAG•CTG triplet repeat expandability and flanking genomic DNA GC content Histone deacetylase complexes promote trinucleotide repeat expansions Msh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in mice Nucleotide excision repair, mismatch repair, and R-loops modulate convergent transcription-induced cell death and repeat instability Transcription elongation and tissue-specific somatic CAG instability.Proteomic-coupled-network analysis of T877A-androgen receptor interactomes can predict clinical prostate cancer outcomes between White (non-Hispanic) and African-American groups MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice Trinucleotide expansion in disease: why is there a length threshold?Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches Modifiers of (CAG)(n) instability in Machado-Joseph disease (MJD/SCA3) transmissions: an association study with DNA replication, repair and recombination genes.The transcription-coupled repair protein ERCC6/CSB also protects against repeat expansion in a mouse model of the fragile X premutation.Repeat instability during DNA repair: Insights from model systems Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis The Repeat Expansion Diseases: The dark side of DNA repair.Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase.Histone deacetylase complexes as caretakers of genome stability.MutSβ and histone deacetylase complexes promote expansions of trinucleotide repeats in human cells.Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.Bidirectional transcription of trinucleotide repeats: roles for excision repair.Crosstalk between MSH2-MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair.Abnormal base excision repair at trinucleotide repeats associated with diseases: a tissue-selective mechanism.Expression levels of DNA replication and repair genes predict regional somatic repeat instability in the brain but are not altered by polyglutamine disease protein expression or age.Mismatch repair enhances convergent transcription-induced cell death at trinucleotide repeats by activating ATR.Convergent transcription through microsatellite repeat tracts induces cell death.RNA toxicity and foci formation in microsatellite expansion diseases.Mechanisms of DNA damage, repair, and mutagenesis.Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.Disease-associated CAG·CTG triplet repeats expand rapidly in non-dividing mouse cells, but cell cycle arrest is insufficient to drive expansion.Age-related length variability of polymorphic CAG repeats.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.

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P2860

Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.

http://www.wikidata.org/entity/Q34021533

description

2011 nî lūn-bûn

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2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին 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

Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

@ast

Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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type

label

Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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prefLabel

Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Xpa deficiency reduces CAG tri ...... sues in a mouse model of SCA1.

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Human Molecular Genetics

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Xpa deficiency reduces CAG tri ...... ssues in a mouse model of SCA1

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P2093

John H Wilson

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Leroy Hubert

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Yunfu Lin

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P2860

Transcription promotes contraction of CAG repeat tracts in human cells

BRCA1/BARD1 inhibition of mRNA 3' processing involves targeted degradation of RNA polymerase II.

Cockayne syndrome group B protein enhances elongation by RNA polymerase II

New insights into repeat instability: role of RNA•DNA hybrids

DNA slip-outs cause RNA polymerase II arrest in vitro: potential implications for genetic instability

Recruitment of the putative transcription-repair coupling factor CSB/ERCC6 to RNA polymerase II elongation complexes

Advances in mechanisms of genetic instability related to hereditary neurological diseases.

DNA damage-induced BARD1 phosphorylation is critical for the inhibition of messenger RNA processing by BRCA1/BARD1 complex.

Trinucleotide repeats that expand in human disease form hairpin structures in vitro

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

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4822-4830

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scholarly article

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10.1093/HMG/DDR421

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24

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20

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2011-09-15T00:00:00Z

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51650508

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21926083

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3221534

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