Evidence map›Paper›PMID 27669035›Full record

ArticleNature structural & molecular biology2016

E4 ligase-specific ubiquitination hubs coordinate DNA double-strand-break repair and apoptosis.

Leena Ackermann, Michael Schell, Wojciech Pokrzywa, Éva Kevei, Anton Gartner, Björn Schumacher, Thorsten Hoppe

Abstract read
In one paragraph

Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Article
  2. Review
  3. Ufd2p promotes efficient crossover formation by destabilizing Top2p during meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Review
  6. Article
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  9. Article
  10. Article
  11. Review
  12. USP7 and VCPCell reports · 2021
    Article
  13. Article
  14. Review
  15. Review
  16. DNA Damaged Induced Cell Death in Oocytes.Molecules (Basel, Switzerland) · 2020
    Review
  17. Review
  18. Review
  19. Article
  20. Review
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.

Leena Ackermann *Institute for Genetics and CECAD Research Center, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Michael Schell *Institute for Genetics and CECAD Research Center, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Wojciech PokrzywaInstitute for Genetics and CECAD Research Center, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Éva KeveiInstitute for Genetics and CECAD Research Center, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Anton GartnerCentre for Gene Regulation and Expression, College of Life Sciences, University of Dundee Scotland.
Björn SchumacherInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.
Thorsten HoppeInstitute for Genetics and CECAD Research Center, University of Cologne, Joseph-Stelzmann Str. 26, 50931 Cologne, Germany.

Funding

Wellcome Trust 090944
6 · The paper itself

Abstract

Multiple protein ubiquitination events at DNA double-strand breaks (DSBs) regulate damage recognition, signaling and repair. It has remained poorly understood how the repair process of DSBs is coordinated with the apoptotic response. Here, we identified the E4 ubiquitin ligase UFD-2 as a mediator of DNA-damage-induced apoptosis in a genetic screen in Caenorhabditis elegans. We found that, after initiation of homologous recombination by RAD-51, UFD-2 forms foci that contain substrate-processivity factors including the ubiquitin-selective segregase CDC-48 (p97), the deubiquitination enzyme ATX-3 (Ataxin-3) and the proteasome. In the absence of UFD-2, RAD-51 foci persist, and DNA damage-induced apoptosis is prevented. In contrast, UFD-2 foci are retained until recombination intermediates are removed by the Holliday-junction-processing enzymes GEN-1, MUS-81 or XPF-1. Formation of UFD-2 foci also requires proapoptotic CEP-1 (p53) signaling. Our findings establish a central role of UFD-2 in the coordination between the DNA-repair process and the apoptotic response.

Indexed as

ApoptosisDNA Breaks, Double-StrandedDNA RepairUbiquitinationAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA DamageGene DeletionRad51 RecombinaseUbiquitin-Protein Ligase ComplexesCaenorhabditis elegans Proteinsrad-51 protein, C elegansRad51 RecombinaseUbiquitin-Protein Ligase Complexesufd-2 protein, C elegans

Identifiers

PMID27669035
PMCPMC5349472

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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.