Amit L Deshmukh, Antonio Porro, Mohiuddin Mohiuddin, Stella Lanni, Gagan B Panigrahi, Marie-Christine Caron, Jean-Yves Masson, Alessandro A Sartori, Christopher E Pearson. J Huntingtons Dis 2021
Times Cited: 10
Times Cited: 10
Times Cited
Times Co-cited
Similarity
90
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Modifiers of Somatic Repeat Instability in Mouse Models of Friedreich Ataxia and the Fragile X-Related Disorders: Implications for the Mechanism of Somatic Expansion in Huntington's Disease.
Xiaonan Zhao, Daman Kumari, Carson J Miller, Geum-Yi Kim, Bruce Hayward, Antonia G Vitalo, Ricardo Mouro Pinto, Karen Usdin. J Huntingtons Dis 2021
Xiaonan Zhao, Daman Kumari, Carson J Miller, Geum-Yi Kim, Bruce Hayward, Antonia G Vitalo, Ricardo Mouro Pinto, Karen Usdin. J Huntingtons Dis 2021
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DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases.
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Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.
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MSH3 modifies somatic instability and disease severity in Huntington's and myotonic dystrophy type 1.
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FAN1 modifies Huntington's disease progression by stabilizing the expanded HTT CAG repeat.
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Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis.
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FAN1 protects against repeat expansions in a Fragile X mouse model.
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A genetic association study of glutamine-encoding DNA sequence structures, somatic CAG expansion, and DNA repair gene variants, with Huntington disease clinical outcomes.
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MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
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Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study.
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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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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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A slipped-CAG DNA-binding small molecule induces trinucleotide-repeat contractions in vivo.
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Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.
Vanessa C Wheeler, Vincent Dion. J Huntingtons Dis 2021
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DNA Mismatch Repair and its Role in Huntington's Disease.
Ravi R Iyer, Anna Pluciennik. J Huntingtons Dis 2021
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Patterns of CAG repeat instability in the central nervous system and periphery in Huntington's disease and in spinocerebellar ataxia type 1.
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Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington's disease knock-in mice is blocked by Mlh1 knock-out.
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Approaches to Sequence the HTT CAG Repeat Expansion and Quantify Repeat Length Variation.
Marc Ciosi, Sarah A Cumming, Afroditi Chatzi, Eloise Larson, William Tottey, Vilija Lomeikaite, Graham Hamilton, Vanessa C Wheeler, Ricardo Mouro Pinto, Seung Kwak,[...]. J Huntingtons Dis 2021
Marc Ciosi, Sarah A Cumming, Afroditi Chatzi, Eloise Larson, William Tottey, Vilija Lomeikaite, Graham Hamilton, Vanessa C Wheeler, Ricardo Mouro Pinto, Seung Kwak,[...]. J Huntingtons Dis 2021
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What is the Pathogenic CAG Expansion Length in Huntington's Disease?
Jasmine Donaldson, Sophie Powell, Nadia Rickards, Peter Holmans, Lesley Jones. J Huntingtons Dis 2021
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The Contribution of Somatic Expansion of the CAG Repeat to Symptomatic Development in Huntington's Disease: A Historical Perspective.
Darren G Monckton. J Huntingtons Dis 2021
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Monika H M Schmidt, Christopher E Pearson. DNA Repair (Amst) 2016
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Drugging DNA Damage Repair Pathways for Trinucleotide Repeat Expansion Diseases.
Caroline L Benn, Karl R Gibson, David S Reynolds. J Huntingtons Dis 2021
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Genetic and Functional Analyses Point to FAN1 as the Source of Multiple Huntington Disease Modifier Effects.
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A genetic screen identifies FAN1, a Fanconi anemia-associated nuclease necessary for DNA interstrand crosslink repair.
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Bidirectional transcription stimulates expansion and contraction of expanded (CTG)*(CAG) repeats.
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Detection of slipped-DNAs at the trinucleotide repeats of the myotonic dystrophy type I disease locus in patient tissues.
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A modifier of Huntington's disease onset at the MLH1 locus.
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Extrahelical (CAG)/(CTG) triplet repeat elements support proliferating cell nuclear antigen loading and MutLα endonuclease activation.
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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.