Evidence map›Paper›PMID 33087278›Full record

ReviewDNA repair2020

Trinucleotide repeat instability via DNA base excision repair.

Yanhao Lai, Jill M Beaver, Eduardo Laverde, Yuan Liu

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. DNA polymerase β suppresses somatic indels at CpG dinucleotides in developing cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yanhao LaiDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States; Biomolecular Sciences Institute, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States.
Jill M BeaverBiochemistry Ph.D. Program, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States.
Eduardo LaverdeBiochemistry Ph.D. Program, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States.
Yuan LiuDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States; Biomolecular Sciences Institute, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States; Biochemistry Ph.D. Program, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States. Electronic address: yualiu@fiu.edu.
Florida International University · US

Funding

Trinucleotide Repeat Instability via DNA Damage and RepairR01ES023569 · NIEHS · FLORIDA INTERNATIONAL UNIVERSITY · PI LIU, YUAN · 2014 to 2018
$1.6M
NIEHS NIH HHS R01 ES023569
6 · The paper itself

Abstract

Trinucleotide repeat (TNR) instability is the cause of over 40 human neurodegenerative diseases and certain types of cancer. TNR instability can result from DNA replication, repair, recombination, and gene transcription. Emerging evidence indicates that DNA base damage and base excision repair (BER) play an active role in regulating somatic TNR instability. These processes may potentially modulate the onset and progression of TNR-related diseases, given that TNRs are hotspots of DNA base damage that are present in mammalian cells with a high frequency. In this review, we discuss the recent advances in our understanding of the molecular mechanisms underlying BER-mediated TNR instability. We initially discuss the roles of the BER pathway and locations of DNA base lesions in TNRs and their interplay with non-B form DNA structures in governing repeat instability. We then discuss how the coordinated activities of BER enzymes can modulate a balance between the removal and addition of TNRs to regulate somatic TNR instability. We further discuss how this balance can be disrupted by the crosstalk between BER and DNA mismatch repair (MMR) machinery resulting in TNR expansion. Finally, we suggest future directions regarding BER-mediated somatic TNR instability and its association with TNR disease prevention and treatment.

Indexed as

DNA RepairTrinucleotide Repeat ExpansionAnimalsDNADNA DamageDNA Mismatch RepairHumansTrinucleotide RepeatsDNADNA base damageDNA base excision repairDNA repair crosstalkTrinucleotide repeat instability

Identifiers

PMID33087278
PMCPMC7586489
OpenAlexW3093705068

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.