ArticlePloS one2013
Instability of CTG repeats is governed by the position of a DNA base lesion through base excision repair.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- DNA Base Damage Repair Crosstalks with Chromatin Structures to Contract Expanded GAA Repeats in Friedreich's Ataxia.Biomolecules · 2024Article
- Suppression of trinucleotide repeat expansion in spermatogenic cells in Huntington's disease.Journal of assisted reproduction and genetics · 2022Article
- Review
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- R-loops promote trinucleotide repeat deletion through DNA base excision repair enzymatic activities.The Journal of biological chemistry · 2020Article
- Trinucleotide repeat instability via DNA base excision repair.DNA repair · 2020Review
- Methods to Study Trinucleotide Repeat Instability Induced by DNA Damage and Repair.Methods in molecular biology (Clifton, N.J.) · 2019Article
- The deoxyribose phosphate lyase of DNA polymerase β suppresses a processive DNA synthesis to prevent trinucleotide repeat instability.Nucleic acids research · 2018Article
- An oxidized abasic lesion inhibits base excision repair leading to DNA strand breaks in a trinucleotide repeat tract.PloS one · 2018Article
- Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018Article
- Modulation of trinucleotide repeat instability by DNA polymerase β polymorphic variant R137Q.PloS one · 2017Article
- Proliferating cell nuclear antigen prevents trinucleotide repeat expansions by promoting repeat deletion and hairpin removal.DNA repair · 2016Article
- Crosstalk between MSH2-MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair.Nature communications · 2016Article
- AP endonuclease 1 prevents trinucleotide repeat expansion via a novel mechanism during base excision repair.Nucleic acids research · 2015Article
- A 5', 8-cyclo-2'-deoxypurine lesion induces trinucleotide repeat deletion via a unique lesion bypass by DNA polymerase β.Nucleic acids research · 2014Article
- APE1 incision activity at abasic sites in tandem repeat sequences.Journal of molecular biology · 2014Article
- Base excision repair of oxidative DNA damage coupled with removal of a CAG repeat hairpin attenuates trinucleotide repeat expansion.Nucleic acids research · 2014Article
- Article
- Article
- Repeat instability during DNA repair: Insights from model systems.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Trinucleotide repeat (TNR) expansions and deletions are associated with human neurodegeneration and cancer. However, their underlying mechanisms remain to be elucidated. Recent studies have demonstrated that CAG repeat expansions can be initiated by oxidative DNA base damage and fulfilled by base excision repair (BER), suggesting active roles for oxidative DNA damage and BER in TNR instability. Here, we provide the first evidence that oxidative DNA damage can induce CTG repeat deletions along with limited expansions in human cells. Biochemical characterization of BER in the context of (CTG)20 repeats further revealed that repeat instability correlated with the position of a base lesion in the repeat tract. A lesion located at the 5'-end of CTG repeats resulted in expansion, whereas a lesion located either in the middle or the 3'-end of the repeats led to deletions only. The positioning effects appeared to be determined by the formation of hairpins at various locations on the template and the damaged strands that were bypassed by DNA polymerase β and processed by flap endonuclease 1 with different efficiency. Our study indicates that the position of a DNA base lesion governs whether TNR is expanded or deleted through BER.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.