Evidence map›Paper›PMID 25428354›Full record

ArticleNucleic acids research2014

A 5', 8-cyclo-2'-deoxypurine lesion induces trinucleotide repeat deletion via a unique lesion bypass by DNA polymerase β.

Meng Xu, Yanhao Lai, Zhongliang Jiang, Michael A Terzidis, Annalisa Masi, Chryssostomos Chatgilialoglu, Yuan Liu

Abstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
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  8. (5'International journal of molecular sciences · 2021
    Article
  9. Review
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  17. Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017
    Review
  18. Article
  19. Article
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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

7 authors.

Meng XuDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW, 8th Street, Miami, FL 33199, USA.
Yanhao LaiDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW, 8th Street, Miami, FL 33199, USA.
Zhongliang JiangDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW, 8th Street, Miami, FL 33199, USA.
Michael A TerzidisISOF, Consiglio Nazionale delle Ricerche, Via P. Gobetti 101, 40129 Bologna, Italy.
Annalisa MasiISOF, Consiglio Nazionale delle Ricerche, Via P. Gobetti 101, 40129 Bologna, Italy.
Chryssostomos ChatgilialogluISOF, Consiglio Nazionale delle Ricerche, Via P. Gobetti 101, 40129 Bologna, Italy Institute of Nanoscience and Nanotechnology, N.C.S.R. 'Demokritos', 15341 Agia, Paraskevi, Athens, Greece.
Yuan LiuDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW, 8th Street, Miami, FL 33199, USA Biomolecular Sciences Institute, School of Integrated Sciences and Humanities, Florida International University, 11200 SW, 8th Street, Miami, FL 33199, USA yualiu@fiu.edu.

Funding

Trinucleotide Repeat Instability via DNA Damage and RepairR01ES023569 · NIEHS · FLORIDA INTERNATIONAL UNIVERSITY · PI LIU, YUAN · 2014 to 2018
$1.6M
NIEHS NIH HHS ES023569NIEHS NIH HHS R01 ES023569
6 · The paper itself

Abstract

5',8-cyclo-2'-deoxypurines (cdPus) are common forms of oxidized DNA lesions resulting from endogenous and environmental oxidative stress such as ionizing radiation. The lesions can only be repaired by nucleotide excision repair with a low efficiency. This results in their accumulation in the genome that leads to stalling of the replication DNA polymerases and poor lesion bypass by translesion DNA polymerases. Trinucleotide repeats (TNRs) consist of tandem repeats of Gs and As and therefore are hotspots of cdPus. In this study, we provided the first evidence that both (5'R)- and (5'S)-5',8-cyclo-2'-deoxyadenosine (cdA) in a CAG repeat tract caused CTG repeat deletion exclusively during DNA lagging strand maturation and base excision repair. We found that a cdA induced the formation of a CAG loop in the template strand, which was skipped over by DNA polymerase β (pol β) lesion bypass synthesis. This subsequently resulted in the formation of a long flap that was efficiently cleaved by flap endonuclease 1, thereby leading to repeat deletion. Our study indicates that accumulation of cdPus in the human genome can lead to TNR instability via a unique lesion bypass by pol β.

Indexed as

DNA DamageDNA RepairDNA ReplicationTrinucleotide RepeatsDeoxyadenosinesDNADNA Polymerase betaFlap EndonucleasesSequence DeletionTemplates, Genetic8,5'-cyclo-2'-deoxyadenosineDeoxyadenosinesDNADNA Polymerase betaFlap EndonucleasesOkazaki fragments

Identifiers

PMID25428354
PMCPMC4267656

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LicenceCC BY
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Registered trials

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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.