Evidence map›Paper›PMID 29599527›Full record

ArticleScientific reports2018

The mitochondrial outer-membrane location of the EXD2 exonuclease contradicts its direct role in nuclear DNA repair.

Fenna Hensen, Amandine Moretton, Selma van Esveld, Géraldine Farge, Johannes N Spelbrink

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. Neuronal ABCA7 deficiency aggravates mitochondrial dysfunction and neurodegeneration in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  10. Split-TurboID enables contact-dependent proximity labeling in cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Article
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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

5 authors at 2 institutions in 2 countries.

Fenna HensenRadboud Center for Mitochondrial Medicine, Department of Paediatrics, Radboudumc, Nijmegen, The Netherlands.
Amandine MorettonUniversité Clermont Auvergne, CNRS/IN2P3, Laboratoire de Physique de Clermont, BP 10448, F-63000, Clermont-Ferrand, France.
Selma van EsveldRadboud Center for Mitochondrial Medicine & Center for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboudumc, Nijmegen, The Netherlands.ORCID 0000-0001-7959-0469
Géraldine FargeUniversité Clermont Auvergne, CNRS/IN2P3, Laboratoire de Physique de Clermont, BP 10448, F-63000, Clermont-Ferrand, France.
Johannes N SpelbrinkRadboud Center for Mitochondrial Medicine, Department of Paediatrics, Radboudumc, Nijmegen, The Netherlands. hans.spelbrink@radboudumc.nl.ORCID 0000-0002-9756-2602
Radboud University Nijmegen · NLCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EXD2 is a recently identified exonuclease that has been implicated in nuclear double-strand break repair. Given our long standing interest in mitochondrial DNA maintenance and indications that EXD2 could also be a mitochondrial protein we sought to determine its cellular localization and possible mitochondrial associated functions. Our results show that EXD2 indeed shows mitochondrial localization, but, surprisingly, is found predominantly associated with the mitochondrial outer-membrane. Gradient purified nuclei show only the faintest hint of EXD2 presence while overexpression of the predicted full-length protein shows exclusive mitochondrial localization. Importantly, induction of double-strand DNA breaks via X-irradiation or Zeocin treatment does not support the notion that EXD2 re-locates to the nucleus following double-strand breaks and thus is unlikely to have a direct role in nuclear DNA repair. Knockdown or overexpression of EXD2 affects the cellular distribution of mitochondria. These results suggest that the reported defects in nuclear DNA repair following EXD2 depletion are likely an indirect consequence of altered mitochondrial dynamics and/or function.

Indexed as

DNA RepairCell Line, TumorCell NucleusDNA Breaks, Double-StrandedExonucleasesHumansMicroscopy, FluorescenceMitochondriaMitochondrial MembranesMitochondrial ProteinsRNA InterferenceRNA, Small InterferingExonucleasesMitochondrial ProteinsRNA, Small Interfering

Identifiers

PMID29599527
PMCPMC5876329
OpenAlexW2803512168

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.