A novel approach to investigate tissue-specific trinucleotide repeat instability.
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A MutSβ-Dependent Contribution of MutSα to Repeat Expansions in Fragile X Premutation Mice?GFP-based fluorescence assay for CAG repeat instability in cultured human cellsGender 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 disordersA selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease miceQuantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liverXpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.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 contentMsh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in miceThe overdue promise of short tandem repeat variation for heritability.Transcription, epigenetics and ameliorative strategies in Huntington's Disease: a genome-wide perspectiveMismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approachesChromosome substitution strain assessment of a Huntington's disease modifier locusThe transcription-coupled repair protein ERCC6/CSB also protects against repeat expansion in a mouse model of the fragile X premutation.Heterozygosity for a hypomorphic Polβ mutation reduces the expansion frequency in a mouse model of the Fragile X-related disorders.Three Huntington's Disease Specific Mutation-Carrying Human Embryonic Stem Cell Lines Have Stable Number of CAG Repeats upon In Vitro Differentiation into Cardiomyocytes.Large expansion of CTG•CAG repeats is exacerbated by MutSβ in human cells.Assessment of copy number variations in the brain genome of schizophrenia patients.Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesisSequence-Level Analysis of the Major European Huntington Disease Haplotype.Effects of Anthocyanins on CAG Repeat Instability and Behaviour in Huntington's Disease R6/1 Mice.Single cell genomics of the brain: focus on neuronal diversity and neuropsychiatric diseases.Mutsβ generates both expansions and contractions in a mouse model of the Fragile X-associated disordersSomatic expansion in mouse and human carriers of fragile X premutation alleles.Neil1 is a genetic modifier of somatic and germline CAG trinucleotide repeat instability in R6/1 mice.Problems and solutions for the analysis of somatic CAG repeat expansion and their relationship to Huntington's disease toxicity.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.Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice.The mismatch repair protein MSH2 is rate limiting for repeat expansion in a fragile X premutation mouse model.What monozygotic twins discordant for phenotype illustrate about mechanisms influencing genetic forms of neurodegeneration.Disease-associated CAG·CTG triplet repeats expand rapidly in non-dividing mouse cells, but cell cycle arrest is insufficient to drive expansion.Cytokine combination therapy prediction for bone remodeling in tissue engineering based on the intracellular signaling pathway.Comparison of Huntington's disease CAG Repeat Length Stability in Human Motor Cortex and Cingulate Gyrus.High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgrounds.Somatic instability of the expanded CTG triplet repeat in myotonic dystrophy type 1 is a heritable quantitative trait and modifier of disease severity.HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction.Detailed analysis of HTT repeat elements in human blood using targeted amplification-free long-read sequencing
P2860
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P2860
A novel approach to investigate tissue-specific trinucleotide repeat instability.
description
2010 nî lūn-bûn
@nan
2010 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մարտին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@ast
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@en
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@nl
type
label
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@ast
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@en
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@nl
prefLabel
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@ast
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@en
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@nl
P2093
P2860
P50
P356
P1433
P1476
A novel approach to investigate tissue-specific trinucleotide repeat instability.
@en
P2093
Edith T Lopez
Ella Dragileva
John R Walker
Jong-Min Lee
Kihwa Kang
Marie-Josee Boily
Michel Cyr
Tim Wiltshire
Vanessa C Wheeler
P2860
P2888
P356
10.1186/1752-0509-4-29
P577
2010-03-19T00:00:00Z
P5875
P6179
1041209784