Evidence map›Paper›PMID 23012265›Full record

ArticleNucleic acids research2012

The dynamics of Ku70/80 and DNA-PKcs at DSBs induced by ionizing radiation is dependent on the complexity of damage.

Pamela Reynolds, Jennifer A Anderson, Jane V Harper, Mark A Hill, Stanley W Botchway, Anthony W Parker, Peter O'Neill

Abstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing 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

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

  1. Pooled it
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  15. The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
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  20. Unraveling the Molecular Impact of Sperm DNA Damage on Human Reproduction.Advances in experimental medicine and biology · 2022
    Article

10 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

7 authors.

Pamela ReynoldsDepartment of Oncology, Gray Institute for Radiation Oncology & Biology, University of Oxford, Oxford OX3 7DQ, UK.
Jennifer A Anderson
Jane V Harper
Mark A Hill
Stanley W Botchway
Anthony W Parker
Peter O'Neill

Funding

Medical Research Council 89975Medical Research Council MC_PC_12001
6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) are biologically one of the most important cellular lesions and possess varying degrees of chemical complexity. The notion that the repairability of more chemically complex DSBs is inefficient led to the concept that the extent of DSB complexity underlies the severity of the biological consequences. The repair of DSBs by non-homologous end joining (NHEJ) has been extensively studied but it remains unknown whether more complex DSBs require a different sub-set of NHEJ protein for their repair compared with simple DSBs. To address this, we have induced DSBs in fluorescently tagged mammalian cells (Ku80-EGFP, DNA-PKcs-YFP or XRCC4-GFP, key proteins in NHEJ) using ultra-soft X-rays (USX) or multi-photon near infrared (NIR) laser irradiation. We have shown in real-time that simple DSBs, induced by USX or NIR microbeam irradiation, are repaired rapidly involving Ku70/80 and XRCC4/Ligase IV/XLF. In contrast, DSBs with greater chemical complexity are repaired slowly involving not only Ku70/80 and XRCC4/Ligase IV/XLF but also DNA-PKcs. Ataxia telangiectasia-mutated inhibition only retards repair of the more chemically complex DSBs which require DNA-PKcs. In summary, the repair of DSBs by NHEJ is highly regulated with pathway choice and kinetics of repair dependent on the chemical complexity of the DSB.

Indexed as

DNA Breaks, Double-StrandedDNA End-Joining RepairRadiation, IonizingAnimalsAntigens, NuclearAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineDNA-Activated Protein KinaseDNA-Binding ProteinsKineticsKu AutoantigenProtein Serine-Threonine KinasesTumor Suppressor ProteinsAntigens, NuclearAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Activated Protein KinaseDNA-Binding ProteinsKu AutoantigenProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID23012265
PMCPMC3510491

What OpenQuestion holds

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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.