S Kang, A Jaworski, K Ohshima, R D Wells. Nat Genet 1995
Times Cited: 308
Times Cited: 308
Times Cited
Times Co-cited
Similarity
Repeat instability: mechanisms of dynamic mutations.
Christopher E Pearson, Kerrie Nichol Edamura, John D Cleary. Nat Rev Genet 2005
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G M Samadashwily, G Raca, S M Mirkin. Nat Genet 1997
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Trinucleotide repeats that expand in human disease form hairpin structures in vitro.
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C H Freudenreich, S M Kantrow, V A Zakian. Science 1998
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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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Inhibition of FEN-1 processing by DNA secondary structure at trinucleotide repeats.
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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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Evidence of cis-acting factors in replication-mediated trinucleotide repeat instability in primate cells.
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OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells.
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(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition.
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Mechanisms of trinucleotide repeat instability during human development.
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Advances in mechanisms of genetic instability related to hereditary neurological diseases.
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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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Alternative structures in duplex DNA formed within the trinucleotide repeats of the myotonic dystrophy and fragile X loci.
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CTG repeat instability and size variation timing in DNA repair-deficient mice.
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Slipped (CTG)*(CAG) repeats can be correctly repaired, escape repair or undergo error-prone repair.
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Replication-dependent instability at (CTG) x (CAG) repeat hairpins in human cells.
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Saccharomyces cerevisiae Srs2 DNA helicase selectively blocks expansions of trinucleotide repeats.
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DNA structures, repeat expansions and human hereditary disorders.
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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 in Escherichia coli enhances instability of (CTG)n triplet repeats from human hereditary diseases.
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Replication fork dynamics and dynamic mutations: the fork-shift model of repeat instability.
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DNA secondary structure: a common and causative factor for expansion in human disease.
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Replication inhibitors modulate instability of an expanded trinucleotide repeat at the myotonic dystrophy type 1 disease locus in human cells.
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Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion.
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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.