I V Kovtun, C T McMurray. Nat Genet 2001
Times Cited: 210
Times Cited: 210
Times Cited
Times Co-cited
Similarity
Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice.
K Manley, T L Shirley, L Flaherty, A Messer. Nat Genet 1999
K Manley, T L Shirley, L Flaherty, A Messer. Nat Genet 1999
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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.
Irina V Kovtun, Yuan Liu, Magnar Bjoras, Arne Klungland, Samuel H Wilson, Cynthia T McMurray. Nature 2007
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Somatic expansion behaviour of the (CTG)n repeat in myotonic dystrophy knock-in mice is differentially affected by Msh3 and Msh6 mismatch-repair proteins.
Walther J A A van den Broek, Marcel R Nelen, Derick G Wansink, Marga M Coerwinkel, Hein te Riele, Patricia J T A Groenen, Bé Wieringa. Hum Mol Genet 2002
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Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum.
Vanessa C Wheeler, Lori-Anne Lebel, Vladimir Vrbanac, Allison Teed, Hein te Riele, Marcy E MacDonald. Hum Mol Genet 2003
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CTG repeat instability and size variation timing in DNA repair-deficient mice.
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(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition.
Barbara A L Owen, Zungyoon Yang, Maoyi Lai, Maciej Gajec, John D Badger, Jeffrey J Hayes, Winfried Edelmann, Raju Kucherlapati, Teresa M Wilson, Cynthia T McMurray. Nat Struct Mol Biol 2005
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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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Repeat instability as the basis for human diseases and as a potential target for therapy.
Arturo López Castel, John D Cleary, Christopher E Pearson. Nat Rev Mol Cell Biol 2010
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Mechanisms of trinucleotide repeat instability during human development.
Cynthia T McMurray. Nat Rev Genet 2010
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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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Msh3 is a limiting factor in the formation of intergenerational CTG expansions in DM1 transgenic mice.
Laurent Foiry, Li Dong, Cédric Savouret, Laurence Hubert, Hein te Riele, Claudine Junien, Geneviève Gourdon. Hum Genet 2006
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Transcription-induced CAG repeat contraction in human cells is mediated in part by transcription-coupled nucleotide excision repair.
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Trinucleotide repeats that expand in human disease form hairpin structures in vitro.
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Transcription promotes contraction of CAG repeat tracts in human cells.
Yunfu Lin, Vincent Dion, John H Wilson. Nat Struct Mol Biol 2006
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Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis.
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Repeat instability: mechanisms of dynamic mutations.
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MSH2-dependent germinal CTG repeat expansions are produced continuously in spermatogonia from DM1 transgenic mice.
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DNA instability in postmitotic neurons.
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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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Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.
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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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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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Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.
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MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
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Somatic and gonadal mosaicism of the Huntington disease gene CAG repeat in brain and sperm.
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CREB-binding protein modulates repeat instability in a Drosophila model for polyQ disease.
Joonil Jung, Nancy Bonini. Science 2007
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MSH2 ATPase domain mutation affects CTG*CAG repeat instability in transgenic mice.
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Slipped (CTG)*(CAG) repeats can be correctly repaired, escape repair or undergo error-prone repair.
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Cockayne syndrome B protein antagonizes OGG1 in modulating CAG repeat length in vivo.
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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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Histone deacetylase complexes promote trinucleotide repeat expansions.
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R loops stimulate genetic instability of CTG.CAG repeats.
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The mismatch repair protein MSH2 is rate limiting for repeat expansion in a fragile X premutation mouse model.
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Chromosome fragility at GAA tracts in yeast depends on repeat orientation and requires mismatch repair.
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The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model.
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Role of mismatch repair enzymes in GAA·TTC triplet-repeat expansion in Friedreich ataxia induced pluripotent stem cells.
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