Evidence map›Paper›PMID 19779458›Full record

ArticleThe EMBO journal2009

ATM and Artemis promote homologous recombination of radiation-induced DNA double-strand breaks in G2.

Andrea Beucher, Julie Birraux, Leopoldine Tchouandong, Olivia Barton, Atsushi Shibata, Sandro Conrad, Aaron A Goodarzi, Andrea Krempler, Penny A Jeggo, Markus Löbrich

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03462212 (A Randomized, Molecular Driven Phase II Trial of Carboplatin-Paclitaxel-Bevacizumab vs Carboplatin-Paclitaxel-Bevacizumab-Rucaparib vs Carboplatin-Paclitaxel-Rucaparib, Selected According to HRD Status, in Patients With Advanced), which is not on this map. Cited by 290 papers.

0numbers the graph read from it
0cells of the map it votes in
290citing papers in PubMed
14.1field-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.

NCT03462212 phase1 / phase2unknown statusnot on this mapstarted 2021, after this paper: background citation

A Randomized, Molecular Driven Phase II Trial of Carboplatin-Paclitaxel-Bevacizumab vs Carboplatin-Paclitaxel-Bevacizumab-Rucaparib vs Carboplatin-Paclitaxel-Rucaparib, Selected According to HRD Status, in Patients With Advanced (Stage III B-C-IV) Ovarian, Primary Peritoneal and Fallopian Tube Cancer Preceded by a Phase I Dose Escalation Study on Rucaparib-Bevacizumab Combination

TypeinterventionalSponsorFondazione Policlinico Universitario Agostino Gemelli IRCCSRan2021 to 2025Enrolled290ConditionsAdvanced (Stage IIIB-C-IV) Ovarian, Primary Peritoneal and Fallopian Tube CancerArmsCarboplatin, Paclitaxel, Bevacizumab, Rucaparib
3 · Its place in the literature

Who cites it

290 citing papers in PubMed, 529 citations in OpenAlex.

  1. Review
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  6. Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025
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  17. Identification of the main barriers to Ku accumulation in chromatin.bioRxiv : the preprint server for biology · 2024
    Article
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  19. Review
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230 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

10 authors at 2 institutions in 2 countries.

Andrea BeucherDarmstadt University of Technology, Radiation Biology and DNA Repair, Darmstadt, Germany.
Julie Birraux
Leopoldine Tchouandong
Olivia Barton
Atsushi Shibata
Sandro Conrad
Aaron A Goodarzi
Andrea Krempler
Penny A Jeggo
Markus Löbrich
Technical University of Darmstadt · DEUniversity of Sussex · GB

Funding

Medical Research Council G0500897
6 · The paper itself

Abstract

Homologous recombination (HR) and non-homologous end joining (NHEJ) represent distinct pathways for repairing DNA double-strand breaks (DSBs). Previous work implicated Artemis and ATM in an NHEJ-dependent process, which repairs a defined subset of radiation-induced DSBs in G1-phase. Here, we show that in G2, as in G1, NHEJ represents the major DSB-repair pathway whereas HR is only essential for repair of approximately 15% of X- or gamma-ray-induced DSBs. In addition to requiring the known HR proteins, Brca2, Rad51 and Rad54, repair of radiation-induced DSBs by HR in G2 also involves Artemis and ATM suggesting that they promote NHEJ during G1 but HR during G2. The dependency for ATM for repair is relieved by depleting KAP-1, providing evidence that HR in G2 repairs heterochromatin-associated DSBs. Although not core HR proteins, ATM and Artemis are required for efficient formation of single-stranded DNA and Rad51 foci at radiation-induced DSBs in G2 with Artemis function requiring its endonuclease activity. We suggest that Artemis endonuclease removes lesions or secondary structures, which inhibit end resection and preclude the completion of HR or NHEJ.

Indexed as

Apoptosis Regulatory ProteinsAtaxia Telangiectasia Mutated ProteinsBRCA2 ProteinCell Cycle ProteinsCells, CulturedDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesDNA RepairDNA Repair EnzymesEndonucleasesFibroblastsG1 PhaseG2 PhaseGene DeletionHeLa CellsApoptosis Regulatory ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanBLID protein, humanBRCA2 ProteinBRCA2 protein, humanCell Cycle ProteinsDCLRE1C protein, humanDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesEndonucleasesHeterochromatinNHEJ1 protein, humanNuclear ProteinsProtein Serine-Threonine KinasesRad51 RecombinaseRAD54L protein, humanReplication Protein ATumor Suppressor Proteins

Identifiers

PMID19779458
PMCPMC2752027
OpenAlexW2119346494

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.