Evidence map›Paper›PMID 20649466›Full record

ReviewAntioxidants & redox signaling2011

Base excision repair and lesion-dependent subpathways for repair of oxidative DNA damage.

David Svilar, Eva M Goellner, Karen H Almeida, Robert W Sobol

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

165 citing papers in PubMed, 267 citations in OpenAlex.

  1. Review
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  9. [Mechanistic research progress on radiotherapy resistance of cancer stem cells].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  10. Review
  11. OGG1 augments the transcriptional activation ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Structural and Functional Insights into UDGs.Protein and peptide letters · 2025
    Review
  16. Review
  17. Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  18. Review
  19. Article
  20. Article

105 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

4 authors at 2 institutions in 1 country.

David SvilarDepartment of Pharmacology & Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Eva M Goellner
Karen H Almeida
Robert W Sobol
University of Pittsburgh · USRhode Island College · US

Funding

UNDERGRADUATE RESEARCH AND SEMINARSP20RR016457 · NCRR · UNIVERSITY OF RHODE ISLAND · PI SHAKARIAN, ALISON M · 2001 to 2011
$35.5M
Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
DNA repair deficient cells for analysisR44GM087798 · NIGMS · TREVIGEN, INC. · PI GEORGE, JAY, SOBOL, ROBERT W · 2010 to 2011
$2.5M
Priority StageP20CA132385 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SOBOL, ROBERT W · 2007 to 2009
$465k
DNA repair deficient human cells for genomic variation analysisR43GM087798 · NIGMS · TREVIGEN, INC. · PI GEORGE, JAY, SOBOL, ROBERT W · 2009 to 2009
$200k
NCI NIH HHS CA132385NCI NIH HHS CA148629NCI NIH HHS R01 CA148629NCRR NIH HHS P20RR016457NIGMS NIH HHS GM087798
6 · The paper itself

Abstract

Nuclear and mitochondrial genomes are under continuous assault by a combination of environmentally and endogenously derived reactive oxygen species, inducing the formation and accumulation of mutagenic, toxic, and/or genome-destabilizing DNA lesions. Failure to resolve these lesions through one or more DNA-repair processes is associated with genome instability, mitochondrial dysfunction, neurodegeneration, inflammation, aging, and cancer, emphasizing the importance of characterizing the pathways and proteins involved in the repair of oxidative DNA damage. This review focuses on the repair of oxidative damage-induced lesions in nuclear and mitochondrial DNA mediated by the base excision repair (BER) pathway in mammalian cells. We discuss the multiple BER subpathways that are initiated by one of 11 different DNA glycosylases of three subtypes: (a) bifunctional with an associated β-lyase activity; (b) monofunctional; and (c) bifunctional with an associated β,δ-lyase activity. These three subtypes of DNA glycosylases all initiate BER but yield different chemical intermediates and hence different BER complexes to complete repair. Additionally, we briefly summarize alternate repair events mediated by BER proteins and the role of BER in the repair of mitochondrial DNA damage induced by ROS. Finally, we discuss the relation of BER and oxidative DNA damage in the onset of human disease.

Indexed as

DNA DamageDNA RepairDNADNA GlycosylasesHumansMolecular StructureNeoplasmsOxidation-ReductionReactive Oxygen SpeciesDNADNA GlycosylasesReactive Oxygen Species

Identifiers

PMID20649466
PMCPMC3096496
OpenAlexW2088713198

What OpenQuestion holds

Textmetadata
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.