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Times Cited: 210
Times Cited: 210
Times Cited
Times Co-cited
Similarity
Somatic expansion of the Huntington's disease CAG repeat in the brain is associated with an earlier age of disease onset.
Meera Swami, Audrey E Hendricks, Tammy Gillis, Tiffany Massood, Jayalakshmi Mysore, Richard H Myers, Vanessa C Wheeler. Hum Mol Genet 2009
Meera Swami, Audrey E Hendricks, Tammy Gillis, Tiffany Massood, Jayalakshmi Mysore, Richard H Myers, Vanessa C Wheeler. Hum Mol Genet 2009
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Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.
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Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study.
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Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches.
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Somatic and gonadal mosaicism of the Huntington disease gene CAG repeat in brain and sperm.
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Intergenerational and striatal CAG repeat instability in Huntington's disease knock-in mice involve different DNA repair genes.
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DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases.
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MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
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Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum.
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Length-dependent gametic CAG repeat instability in the Huntington's disease knock-in mouse.
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A genetic association study of glutamine-encoding DNA sequence structures, somatic CAG expansion, and DNA repair gene variants, with Huntington disease clinical outcomes.
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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.
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A novel approach to investigate tissue-specific trinucleotide repeat instability.
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FAN1 modifies Huntington's disease progression by stabilizing the expanded HTT CAG repeat.
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Instability of highly expanded CAG repeats in mice transgenic for the Huntington's disease mutation.
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Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice.
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MSH3 modifies somatic instability and disease severity in Huntington's and myotonic dystrophy type 1.
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Msh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in mice.
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The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington's disease.
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Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice.
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Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington's Disease.
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Venezuelan kindreds reveal that genetic and environmental factors modulate Huntington's disease age of onset.
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Length of Uninterrupted CAG, Independent of Polyglutamine Size, Results in Increased Somatic Instability, Hastening Onset of Huntington Disease.
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Patterns of CAG repeat instability in the central nervous system and periphery in Huntington's disease and in spinocerebellar ataxia type 1.
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Aberrant splicing of HTT generates the pathogenic exon 1 protein in Huntington disease.
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A modifier of Huntington's disease onset at the MLH1 locus.
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Pms2 is a genetic enhancer of trinucleotide CAG.CTG repeat somatic mosaicism: implications for the mechanism of triplet repeat expansion.
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Targeting Huntingtin Expression in Patients with Huntington's Disease.
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A new model for prediction of the age of onset and penetrance for Huntington's disease based on CAG length.
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CAG repeat expansion in Huntington disease determines age at onset in a fully dominant fashion.
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Trinucleotide repeats that expand in human disease form hairpin structures in vitro.
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Stoichiometry of base excision repair proteins correlates with increased somatic CAG instability in striatum over cerebellum in Huntington's disease transgenic mice.
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(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.