ReviewDNA repair2017
Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.
Review in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
27 citing papers in PubMed.
- DNA extrusion size determines pathway choice during CAG repeat expansion.Nucleic acids research · 2025Article
- Isotopic H/D Exchange in Hydrogen Bonds Between the Nitrogenous Bases of the CAG Repeat Tract Makes It Possible to Stabilize Its Expansion in theBiomedicines · 2025Article
- Deaminase-Driven Reverse Transcription Mutagenesis in Oncogenesis: Critical Analysis of Transcriptional Strand Asymmetries of Single Base Substitution Signatures.International journal of molecular sciences · 2025Review
- A single CAA interrupt in a DNA three-way junction containing a CAG repeat hairpin results in parity-dependent trapping.Nucleic acids research · 2024Article
- Massive contractions of myotonic dystrophy type 2-associated CCTG tetranucleotide repeats occur via double-strand break repair with distinct requirements for DNA helicases.G3 (Bethesda, Md.) · 2024Article
- HTLV-1 bZIP factor impairs DNA mismatch repair system.Biochemical and biophysical research communications · 2023Article
- Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks.Nature communications · 2023Article
- Heterogeneous migration routes of DNA triplet repeat slip-outs.Biophysical reports · 2022Article
- Restarted replication forks are error-prone and cause CAG repeat expansions and contractions.PLoS genetics · 2021Article
- Secondary structural choice of DNA and RNA associated with CGG/CCG trinucleotide repeat expansion rationalizes the RNA misprocessing in FXTAS.Scientific reports · 2021Article
- Conformational and migrational dynamics of slipped-strand DNA three-way junctions containing trinucleotide repeats.Nature communications · 2021Article
- 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.Journal of Huntington's disease · 2021Review
- All three mammalian MutL complexes are required for repeat expansion in a mouse cell model of the Fragile X-related disorders.PLoS genetics · 2020Article
- Review
- Defects in the GINS complex increase the instability of repetitive sequences via a recombination-dependent mechanism.PLoS genetics · 2019Article
- Dynamic DNA Energy Landscapes and Substrate Complexity in Triplet Repeat Expansion and DNA Repair.Biomolecules · 2019Article
- Mismatch Recognition byInternational journal of molecular sciences · 2019Article
- The role of fork stalling and DNA structures in causing chromosome fragility.Genes, chromosomes & cancer · 2019Review
- The impact of poly-A microsatellite heterologies in meiotic recombination.Life science alliance · 2019Article
- MutSγ-Induced DNA Conformational Changes Provide Insights into Its Role in Meiotic Recombination.Biophysical journal · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Expansion of simple triplet repeats (TNR) underlies more than 30 severe degenerative diseases. There is a good understanding of the major pathways generating an expansion, and the associated polymerases that operate during gap filling synthesis at these "difficult to copy" sequences. However, the mechanism by which a TNR is repaired depends on the type of lesion, the structural features imposed by the lesion, the assembled replication/repair complex, and the polymerase that encounters it. The relationships among these parameters are exceptionally complex and how they direct pathway choice is poorly understood. In this review, we consider the properties of polymerases, and how encounters with GC-rich or abnormal structures might influence polymerase choice and the success of replication and repair. Insights over the last three years have highlighted new mechanisms that provide interesting choices to consider in protecting genome stability.
Indexed as
Identifiers
What Socratic 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 Socratic graph.