ReviewAnnual review of biochemistry2015
DNA triplet repeat expansion and mismatch repair.
Review in Annual review of biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
74 citing papers in PubMed, 129 citations in OpenAlex.
- Mapping Patterns of G-Quadruplex-Forming Sequence Conservation in Primates.Journal of molecular evolution · 2026Article
- DNA extrusion size determines pathway choice during CAG repeat expansion.Nucleic acids research · 2025Article
- Emerging drivers of DNA repeat expansions.Biochemical Society transactions · 2025Review
- Localization of Potential Energy in Hydrogen Bonds of theInternational journal of molecular sciences · 2025Article
- Advances on the Mechanisms and Therapeutic Strategies in Non-coding CGG Repeat Expansion Diseases.Molecular neurobiology · 2024Review
- Structural and Dynamical Properties of Nucleic Acid Hairpins Implicated in Trinucleotide Repeat Expansion Diseases.Biomolecules · 2024Review
- A single CAA interrupt in a DNA three-way junction containing a CAG repeat hairpin results in parity-dependent trapping.Nucleic acids research · 2024Article
- RNA structure in alternative splicing regulation: from mechanism to therapy.Acta biochimica et biophysica Sinica · 2024Review
- ULTRA-Effective Labeling of Repetitive Genomic Sequence.bioRxiv : the preprint server for biology · 2024Article
- MRE11A: a novel negative regulator of human DNA mismatch repair.Cellular & molecular biology letters · 2024Article
- ULTRA-effective labeling of tandem repeats in genomic sequence.Bioinformatics advances · 2024Article
- Tandem MutSβ binding to long extruded DNA trinucleotide repeats underpins pathogenic expansions.bioRxiv : the preprint server for biology · 2023Article
- Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.Nucleic acids research · 2023Article
- R-LOOPs on Short Tandem Repeat Expansion Disorders in Neurodegenerative Diseases.Molecular neurobiology · 2023Review
- FAN1 removes triplet repeat extrusions via a PCNA- and RFC-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- Frustration Between Preferred States of Complementary Trinucleotide Repeat DNA Hairpins Anticorrelates with Expansion Disease Propensity.Journal of molecular biology · 2023Article
- Dynamic alternative DNA structures in biology and disease.Nature reviews. Genetics · 2023Review
- ORC6, a novel prognostic biomarker, correlates with T regulatory cell infiltration in prostate adenocarcinoma: a pan-cancer analysis.BMC cancer · 2023Article
- How sequence alterations enhance the stability and delay expansion of DNA triplet repeat domains.QRB discovery · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
DNA mismatch repair is a conserved antimutagenic pathway that maintains genomic stability through rectification of DNA replication errors and attenuation of chromosomal rearrangements. Paradoxically, mutagenic action of mismatch repair has been implicated as a cause of triplet repeat expansions that cause neurological diseases such as Huntington disease and myotonic dystrophy. This mutagenic process requires the mismatch recognition factor MutSβ and the MutLα (and/or possibly MutLγ) endonuclease, and is thought to be triggered by the transient formation of unusual DNA structures within the expanded triplet repeat element. This review summarizes the current knowledge of DNA mismatch repair involvement in triplet repeat expansion, which encompasses in vitro biochemical findings, cellular studies, and various in vivo transgenic animal model experiments. We present current mechanistic hypotheses regarding mismatch repair protein function in mediating triplet repeat expansions and discuss potential therapeutic approaches targeting the mismatch repair pathway.
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What OpenQuestion holds
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.