Evidence map›Paper›PMID 27890643›Full record

ReviewFree radical biology & medicine2017

Coordination of DNA single strand break repair.

Rachel Abbotts, David M Wilson

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
–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

124 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Multilevel Mechanisms of Cancer Drug Resistance.International journal of molecular sciences · 2024
    Pooled it
  2. Article
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  4. Article
  5. Review
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  9. The role of sperm DNA fragmentation in reproduction: a SWOT analysis.Journal of assisted reproduction and genetics · 2025
    Review
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  11. Article
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  14. Article
  15. Article
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  18. Article
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  20. Review

64 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

2 authors.

Rachel AbbottsLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA.
David M WilsonLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: wilsonda@mail.nih.gov.

Funding

Base Excision DNA Repair in Disease Susceptibility and TreatmentZIAAG000750 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.4M
Oxidative DNA Damage Repair in Premature Aging and NeurodegenerationZIAAG000751 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.3M
Intramural NIH HHS ZIA AG000751
6 · The paper itself

Abstract

The genetic material of all organisms is susceptible to modification. In some instances, these changes are programmed, such as the formation of DNA double strand breaks during meiotic recombination to generate gamete variety or class switch recombination to create antibody diversity. However, in most cases, genomic damage is potentially harmful to the health of the organism, contributing to disease and aging by promoting deleterious cellular outcomes. A proportion of DNA modifications are caused by exogenous agents, both physical (namely ultraviolet sunlight and ionizing radiation) and chemical (such as benzopyrene, alkylating agents, platinum compounds and psoralens), which can produce numerous forms of DNA damage, including a range of "simple" and helix-distorting base lesions, abasic sites, crosslinks and various types of phosphodiester strand breaks. More significant in terms of frequency are endogenous mechanisms of modification, which include hydrolytic disintegration of DNA chemical bonds, attack by reactive oxygen species and other byproducts of normal cellular metabolism, or incomplete or necessary enzymatic reactions (such as topoisomerases or repair nucleases). Both exogenous and endogenous mechanisms are associated with a high risk of single strand breakage, either produced directly or generated as intermediates of DNA repair. This review will focus upon the creation, consequences and resolution of single strand breaks, with a particular focus on two major coordinating repair proteins: poly(ADP-ribose) polymerase 1 (PARP1) and X-ray repair cross-complementing protein 1 (XRCC1).

Indexed as

DNA Breaks, Single-StrandedDNA DamageDNA RepairAnimalsBenzopyrenesHumansNervous System DiseasesPoly (ADP-Ribose) Polymerase-1Radiation, IonizingReactive Oxygen SpeciesSunlightX-ray Repair Cross Complementing Protein 1BenzopyrenesPoly (ADP-Ribose) Polymerase-1Reactive Oxygen SpeciesX-ray Repair Cross Complementing Protein 1AgingDNA repairNeurodegenerationOxidative DNA damagePARP1XRCC1

Identifiers

PMID27890643
PMCPMC5443707

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.