Irina V Kovtun, Yuan Liu, Magnar Bjoras, Arne Klungland, Samuel H Wilson, Cynthia T McMurray. Nature 2007
Times Cited: 329
Times Cited: 329
Times Cited
Times Co-cited
Similarity
Suppression of Somatic Expansion Delays the Onset of Pathophysiology in a Mouse Model of Huntington's Disease.
Helen Budworth, Faye R Harris, Paul Williams, Do Yup Lee, Amy Holt, Jens Pahnke, Bartosz Szczesny, Karina Acevedo-Torres, Sylvette Ayala-Peña, Cynthia T McMurray. PLoS Genet 2015
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Mechanisms of trinucleotide repeat instability during human development.
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Neil1 is a genetic modifier of somatic and germline CAG trinucleotide repeat instability in R6/1 mice.
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DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases.
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Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study.
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Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice.
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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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Coordination between polymerase beta and FEN1 can modulate CAG repeat expansion.
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Somatic expansion of the Huntington's disease CAG repeat in the brain is associated with an earlier age of disease onset.
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Repeat instability during DNA repair: Insights from model systems.
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Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum.
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Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis.
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Crosstalk between MSH2-MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair.
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MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
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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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DNA instability in postmitotic neurons.
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Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.
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A polymorphism in the MSH3 mismatch repair gene is associated with the levels of somatic instability of the expanded CTG repeat in the blood DNA of myotonic dystrophy type 1 patients.
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DNA base excision repair: a mechanism of trinucleotide repeat expansion.
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Repeat instability as the basis for human diseases and as a potential target for therapy.
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Trinucleotide repeats that expand in human disease form hairpin structures in vitro.
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The role of break-induced replication in large-scale expansions of (CAG)n/(CTG)n repeats.
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Huntingtin is a scaffolding protein in the ATM oxidative DNA damage response complex.
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Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
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Msh3 is a limiting factor in the formation of intergenerational CTG expansions in DM1 transgenic mice.
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