Joonil Jung, Nancy Bonini. Science 2007
Times Cited: 110
Times Cited: 110
Times Cited
Times Co-cited
Similarity
Transcription-induced CAG repeat contraction in human cells is mediated in part by transcription-coupled nucleotide excision repair.
Yunfu Lin, John H Wilson. Mol Cell Biol 2007
Yunfu Lin, John H Wilson. Mol Cell Biol 2007
40
Transcription promotes contraction of CAG repeat tracts in human cells.
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Yunfu Lin, Vincent Dion, John H Wilson. Nat Struct Mol Biol 2006
38
OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.
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Repeat instability: mechanisms of dynamic mutations.
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Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice.
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Dnmt1 deficiency promotes CAG repeat expansion in the mouse germline.
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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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Transcription destabilizes triplet repeats.
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Repeat instability as the basis for human diseases and as a potential target for therapy.
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Xpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.
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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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Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum.
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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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R loops stimulate genetic instability of CTG.CAG repeats.
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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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CTCF cis-regulates trinucleotide repeat instability in an epigenetic manner: a novel basis for mutational hot spot determination.
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Bidirectional transcription stimulates expansion and contraction of expanded (CTG)*(CAG) repeats.
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Instability and chromatin structure of expanded trinucleotide repeats.
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18
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14
Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis.
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A persistent RNA.DNA hybrid formed by transcription of the Friedreich ataxia triplet repeat in live bacteria, and by T7 RNAP in vitro.
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14
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Genome-wide demethylation destabilizes CTG.CAG trinucleotide repeats in mammalian cells.
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