Zhi Yang, Rachel Lau, Julien L Marcadier, David Chitayat, Christopher E Pearson. Am J Hum Genet 2003
Times Cited: 60
Times Cited: 60
Times Cited
Times Co-cited
Similarity
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Christopher E Pearson, Kerrie Nichol Edamura, John D Cleary. Nat Rev Genet 2005
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Evidence of cis-acting factors in replication-mediated trinucleotide repeat instability in primate cells.
John D Cleary, Kerrie Nichol, Yuh-Hwa Wang, Christopher E Pearson. Nat Genet 2002
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Transcription promotes contraction of CAG repeat tracts in human cells.
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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 affect DNA replication in vivo.
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Replication and expansion of trinucleotide repeats in yeast.
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MSH2-dependent germinal CTG repeat expansions are produced continuously in spermatogonia from DM1 transgenic mice.
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Huntington disease expansion mutations in humans can occur before meiosis is completed.
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Transgenic mice carrying large human genomic sequences with expanded CTG repeat mimic closely the DM CTG repeat intergenerational and somatic instability.
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Chemically induced increases and decreases in the rate of expansion of a CAG*CTG triplet repeat.
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Replication-dependent instability at (CTG) x (CAG) repeat hairpins in human cells.
Guoqi Liu, Xiaomi Chen, John J Bissler, Richard R Sinden, Michael Leffak. Nat Chem Biol 2010
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Stability of a CTG/CAG trinucleotide repeat in yeast is dependent on its orientation in the genome.
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Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.
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Msh3 is a limiting factor in the formation of intergenerational CTG expansions in DM1 transgenic mice.
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Mutagenic stress modulates the dynamics of CTG repeat instability associated with myotonic dystrophy type 1.
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Instability of highly expanded CAG repeats in mice transgenic for the Huntington's disease mutation.
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Structural analysis of slipped-strand DNA (S-DNA) formed in (CTG)n. (CAG)n repeats from the myotonic dystrophy locus.
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Replication fork dynamics and dynamic mutations: the fork-shift model of repeat instability.
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MSH2 ATPase domain mutation affects CTG*CAG repeat instability in transgenic mice.
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Slipping while sleeping? Trinucleotide repeat expansions in germ cells.
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Human MSH2 binds to trinucleotide repeat DNA structures associated with neurodegenerative diseases.
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Expansions of CAG repeat tracts are frequent in a yeast mutant defective in Okazaki fragment maturation.
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Recombination-induced CAG trinucleotide repeat expansions in yeast involve the MRE11-RAD50-XRS2 complex.
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Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.
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Alternative structures in duplex DNA formed within the trinucleotide repeats of the myotonic dystrophy and fragile X loci.
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Myotonic dystrophy patients have larger CTG expansions in skeletal muscle than in leukocytes.
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Cis-acting modifiers of expanded CAG/CTG triplet repeat expandability: associations with flanking GC content and proximity to CpG islands.
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Slipped-strand DNAs formed by long (CAG)*(CTG) repeats: slipped-out repeats and slip-out junctions.
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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.