I V Kovtun, C T McMurray. Nat Genet 2001
Times Cited: 209
Times Cited: 209
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
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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.
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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.
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Cédric Savouret, Edith Brisson, Jeroen Essers, Roland Kanaar, Albert Pastink, Hein te Riele, Claudine Junien, Geneviève Gourdon. EMBO J 2003
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Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum.
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(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition.
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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.
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Msh3 is a limiting factor in the formation of intergenerational CTG expansions in DM1 transgenic mice.
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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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Transcription promotes contraction of CAG repeat tracts in human cells.
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Trinucleotide repeats that expand in human disease form hairpin structures in vitro.
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Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis.
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MSH2-dependent germinal CTG repeat expansions are produced continuously in spermatogonia from DM1 transgenic 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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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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MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
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CREB-binding protein modulates repeat instability in a Drosophila model for polyQ disease.
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Histone deacetylase complexes promote trinucleotide repeat expansions.
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