ReviewBiochemical Society transactions2025
Emerging drivers of DNA repeat expansions.
Review in Biochemical Society transactions, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Short Tandem Repeat 3D Structure Database (STR3SD): A Resource for Structural Biology Research of Short Tandem Repeats in Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Replication associated nuclear DNA mismatch repair across kingdoms.Biochemical Society transactions · 2026Review
- Evidence that MutSβ repairs indels generated by mispair initiated template slippage.DNA repair · 2026Article
- Slippage reconfiguration of trinucleotide repeat hairpins impedes resolution by human replication protein A.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Expansions of short tandem repeats (STRs) are the cause of a class of human hereditary disorders called repeat expansion diseases (REDs). Most REDs are neurodegenerative or neurodevelopmental diseases such as Huntington's disease, myotonic dystrophy, fragile X syndrome, and Friedreich's ataxia. Some common neurodegenerative diseases, including Alzheimer's and Parkinson's disease, have also been associated with STR expansions. Many cellular processes such as meiotic recombination, DNA replication, and mismatch repair have been shown to promote STR instability. However, STR instability is likely the result of a variety of factors, and many questions regarding this phenomenon remain to be answered. In this review, we summarize recent studies that propose DNA single-strand breaks as drivers of large-scale STR instability, in both dividing and non-dividing cells, and discuss additional evidence that supports this model. We also highlight the FANCD2- and FANCI-associated nuclease 1 protein, which was shown to be the strongest genetic modifier of several REDs.
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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.