ArticleDNA repair2012
In vitro repair of DNA hairpins containing various numbers of CAG/CTG trinucleotide repeats.
Article in DNA repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed.
- Review
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- DNA Mismatch Repair and its Role in Huntington's Disease.Journal of Huntington's disease · 2021Review
- HDAC3 deacetylates the DNA mismatch repair factor MutSβ to stimulate triplet repeat expansions.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A slipped-CAG DNA-binding small molecule induces trinucleotide-repeat contractions in vivo.Nature genetics · 2020Article
- Review
- DNA mismatch repair in trinucleotide repeat instability.Science China. Life sciences · 2017Review
- MutSβ promotes trinucleotide repeat expansion by recruiting DNA polymerase β to nascent (CAG)n or (CTG)n hairpins for error-prone DNA synthesis.Cell research · 2016Article
- Absence of MutSβ leads to the formation of slipped-DNA for CTG/CAG contractions at primate replication forks.DNA repair · 2016Article
- The Repeat Expansion Diseases: The dark side of DNA repair.DNA repair · 2015Review
- DNA triplet repeat expansion and mismatch repair.Annual review of biochemistry · 2015Review
- Base excision repair of oxidative DNA damage coupled with removal of a CAG repeat hairpin attenuates trinucleotide repeat expansion.Nucleic acids research · 2014Article
- The dual nature of mismatch repair as antimutator and mutator: for better or for worse.Frontiers in genetics · 2014Review
- Coordinated processing of 3' slipped (CAG)n/(CTG)n hairpins by DNA polymerases β and δ preferentially induces repeat expansions.The Journal of biological chemistry · 2013Article
- Trinucleotide repeat expansions catalyzed by human cell-free extracts.Cell research · 2013Article
- The Werner syndrome protein promotes CAG/CTG repeat stability by resolving large (CAG)(n)/(CTG)(n) hairpins.The Journal of biological chemistry · 2012Article
- Repeat instability during DNA repair: Insights from model systems.Critical reviews in biochemistry and molecular biologyReview
- Expanded complexity of unstable repeat diseases.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Expansion of CAG/CTG trinucleotide repeats (TNRs) in humans is associated with a number of neurological and neurodegenerative disorders including Huntington's disease. Increasing evidence suggests that formation of a stable DNA hairpin within CAG/CTG repeats during DNA metabolism leads to TNR instability. However, the molecular mechanism by which cells recognize and repair CAG/CTG hairpins is largely unknown. Recent studies have identified a novel DNA repair pathway specifically removing (CAG)(n)/(CTG)(n) hairpins, which is considered a major mechanism responsible for TNR instability. The hairpin repair (HPR) system targets the repeat tracts for incisions in the nicked strand in an error-free manner. To determine the substrate spectrum of the HPR system and its ability to process smaller hairpins, which may be the intermediates for CAG/CTG expansions, we constructed a series of CAG/CTG hairpin heteroduplexes containing different numbers of repeats (from 5 to 25) and examined their repair in human nuclear extracts. We show here that although repair efficiencies differ slightly among these substrates, removal of the individual hairpin structures all involve endonucleolytic incisions within the repeat tracts in the nicked DNA strand. Analysis of the repair intermediates defined specific incision sites for each substrate, which were all located within the repeat regions. Mismatch repair proteins are not required for, nor do they inhibit, the processing of smaller hairpin structures. These results suggest that the HPR system ensures CAG/CTG stability primarily by removing various sizes of (CAG)(n)/(CTG)(n) hairpin structures during DNA metabolism.
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