Evidence map›Paper›PMID 28132842›Full record

ArticleMolecular cell2017

DNA Double-Strand Break Resection Occurs during Non-homologous End Joining in G1 but Is Distinct from Resection during Homologous Recombination.

Ronja Biehs, Monika Steinlage, Olivia Barton, Szilvia Juhász, Julia Künzel, Julian Spies, Atsushi Shibata, Penny A Jeggo, Markus Löbrich

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 209 citations in OpenAlex.

  1. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
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  11. THE GID COMPLEX REGULATES DNA END PROCESSING DURING DNA DOUBLE-STRAND BREAK REPAIR BY NONHOMOLOGOUS END JOINING.Transactions of the American Clinical and Climatological Association · 2025
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77 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

9 authors at 3 institutions in 3 countries.

Ronja BiehsRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Monika SteinlageRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Olivia BartonRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Szilvia JuhászRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Julia KünzelRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Julian SpiesRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Atsushi ShibataGenome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, UK; Advanced Scientific Research Leaders Development Unit, Gunma University, Maebashi, Gunma 371-8511, Japan. Electronic address: shibata.at@gunma-u.ac.jp.
Penny A JeggoGenome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, UK. Electronic address: p.a.jeggo@sussex.ac.uk.
Markus LöbrichRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany. Electronic address: lobrich@bio.tu-darmstadt.de.
Technical University of Darmstadt · DEGunma University · JPUniversity of Sussex · GB

Funding

Medical Research Council G0500897Medical Research Council G1000050
6 · The paper itself

Abstract

Canonical non-homologous end joining (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cells with biphasic kinetics. We show that DSBs repaired with slow kinetics, including those localizing to heterochromatic regions or harboring additional lesions at the DSB site, undergo resection prior to repair by c-NHEJ and not alt-NHEJ. Resection-dependent c-NHEJ represents an inducible process during which Plk3 phosphorylates CtIP, mediating its interaction with Brca1 and promoting the initiation of resection. Mre11 exonuclease, EXD2, and Exo1 execute resection, and Artemis endonuclease functions to complete the process. If resection does not commence, then repair can ensue by c-NHEJ, but when executed, Artemis is essential to complete resection-dependent c-NHEJ. Additionally, Mre11 endonuclease activity is dispensable for resection in G1. Thus, resection in G1 differs from the process in G2 that leads to homologous recombination. Resection-dependent c-NHEJ significantly contributes to the formation of deletions and translocations in G1, which represent important initiating events in carcinogenesis.

Indexed as

DNA Breaks, Double-StrandedBRCA1 ProteinCarrier ProteinsCell NucleusDNA-Binding ProteinsDNA End-Joining RepairDNA Repair EnzymesEndodeoxyribonucleasesEndonucleasesExodeoxyribonucleasesG1 PhaseG2 PhaseGene DeletionHeLa CellsHumansKineticsBRCA1 ProteinBRCA1 protein, humanCarrier ProteinsDCLRE1C protein, humanDNA-Binding ProteinsDNA Repair EnzymesEndodeoxyribonucleasesEndonucleasesEXO1 protein, humanExodeoxyribonucleasesMRE11 Homologue ProteinMRE11 protein, humanNuclear ProteinsPLK3 protein, humanPolo-like KinasesProtein Serine-Threonine KinasesRBBP8 protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsDNA double-strand breaksnon-homologous end joiningnucleasesresection

Identifiers

PMID28132842
PMCPMC5316416
OpenAlexW2580248979

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.