Evidence map›Paper›PMID 20951653›Full record

ArticleDNA repair2011

Factors that influence telomeric oxidative base damage and repair by DNA glycosylase OGG1.

David B Rhee, Avik Ghosh, Jian Lu, Vilhelm A Bohr, Yie Liu

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Telomere Biology and Thoracic Aortic Aneurysm.International journal of molecular sciences · 2017
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Observational
  6. Review
  7. Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Telomere Attrition in Chronic Kidney Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    Review
  17. Article
  18. Long-Term Exposure to Nanosized TiOInternational journal of molecular sciences · 2021
    Article
  19. Review
  20. Review

12 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

David B RheeLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States.
Avik Ghosh
Jian Lu
Vilhelm A Bohr
Yie Liu
National Institutes of Health · USNational Institute on Aging · US

Funding

Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
The role of DNA damage and repair at telomeresZIAAG000744 · NIA · NATIONAL INSTITUTE ON AGING · PI LIU, YIE · 2009 to 2016
$3.9M
Intramural NIH HHS ZIA AG000744
6 · The paper itself

Abstract

Telomeres are nucleoprotein complexes at the ends of linear chromosomes in eukaryotes, and are essential in preventing chromosome termini from being recognized as broken DNA ends. Telomere shortening has been linked to cellular senescence and human aging, with oxidative stress as a major contributing factor. 7,8-Dihydro-8-oxogaunine (8-oxodG) is one of the most abundant oxidative guanine lesions, and 8-oxoguanine DNA glycosylase (OGG1) is involved in its removal. In this study, we examined if telomeric DNA is particularly susceptible to oxidative base damage and if telomere-specific factors affect the incision of oxidized guanines by OGG1. We demonstrated that telomeric TTAGGG repeats were more prone to oxidative base damage and repaired less efficiently than non-telomeric TG repeats in vivo. We also showed that the 8-oxodG-incision activity of OGG1 is similar in telomeric and non-telomeric double-stranded substrates. In addition, telomere repeat binding factors TRF1 and TRF2 do not impair OGG1 incision activity. Yet, 8-oxodG in some telomere structures (e.g., fork-opening, 3'-overhang, and D-loop) were less effectively excised by OGG1, depending upon its position in these substrates. Collectively, our data indicate that the sequence context of telomere repeats and certain telomere configurations may contribute to telomere vulnerability to oxidative DNA damage processing.

Indexed as

DNA Repair8-Hydroxy-2'-DeoxyguanosineAnimalsCells, CulturedDeoxyguanosineDNADNA DamageDNA GlycosylasesDNA, Single-StrandedHumansMiceOxidative StressRecombinant ProteinsTelomereTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 28-Hydroxy-2'-DeoxyguanosineDeoxyguanosineDNADNA GlycosylasesDNA, Single-Strandedoxoguanine glycosylase 1, humanRecombinant ProteinsTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 2

Identifiers

PMID20951653
PMCPMC3010491
OpenAlexW2107332686

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.