Evidence map›Paper›PMID 26160886›Full record

ArticleNucleic acids research2015

EXO1 is critical for embryogenesis and the DNA damage response in mice with a hypomorphic Nbs1 allele.

Katrin Rein, Diana A Yanez, Berta Terré, Lluís Palenzuela, Suvi Aivio, Kaichun Wei, Winfried Edelmann, Jeremy M Stark, Travis H Stracker

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Katrin ReinInstitute for Research in Biomedicine (IRB Barcelona), Barcelona 08028, Spain.
Diana A YanezDepartment of Radiation Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
Berta TerréInstitute for Research in Biomedicine (IRB Barcelona), Barcelona 08028, Spain.
Lluís PalenzuelaInstitute for Research in Biomedicine (IRB Barcelona), Barcelona 08028, Spain.
Suvi AivioInstitute for Research in Biomedicine (IRB Barcelona), Barcelona 08028, Spain.
Kaichun WeiAlbert Einstein College of Medicine, Department of Cell Biology, Bronx, NY 10461, USA.
Winfried EdelmannAlbert Einstein College of Medicine, Department of Cell Biology, Bronx, NY 10461, USA.
Jeremy M StarkDepartment of Radiation Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
Travis H StrackerInstitute for Research in Biomedicine (IRB Barcelona), Barcelona 08028, Spain Travis.Stracker@irbbarcelona.org.
Institute for Research in Biomedicine · ESAlbert Einstein College of Medicine · USBeckman Research InstituteCity of Hope · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSR01CA076329 · NCI · YESHIVA UNIVERSITY · PI EDELMANN, WINFRIED · 1998 to 2017
$6.9M
The Role of Late MMR Proteins in DNA Repair and CancerR01CA093484 · NCI · YESHIVA UNIVERSITY · PI EDELMANN, WINFRIED · 2002 to 2011
$3.7M
Mechanistic steps of homologous repair in mammalian cellsR01CA120954 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI STARK, JEREMY MICHAEL · 2006 to 2016
$2.2M
Mismatch repair in V region mutation and isotype switchingR01AI112335 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SCHARFF, MATTHEW D · 2014 to 2017
$1.5M
NCI NIH HHS 2R01CA120954/3R01CA120954-08SNCI NIH HHS CA76329NCI NIH HHS CA93484NCI NIH HHS P30 CA013330NCI NIH HHS R01 CA076329NCI NIH HHS R01 CA120954NIAID NIH HHS R01 AI112335
6 · The paper itself

Abstract

The maintenance of genome stability is critical for the suppression of diverse human pathologies that include developmental disorders, premature aging, infertility and predisposition to cancer. The DNA damage response (DDR) orchestrates the appropriate cellular responses following the detection of lesions to prevent genomic instability. The MRE11 complex is a sensor of DNA double strand breaks (DSBs) and plays key roles in multiple aspects of the DDR, including DNA end resection that is critical for signaling and DNA repair. The MRE11 complex has been shown to function both upstream and in concert with the 5'-3' exonuclease EXO1 in DNA resection, but it remains unclear to what extent EXO1 influences DSB responses independently of the MRE11 complex. Here we examine the genetic relationship of the MRE11 complex and EXO1 during mammalian development and in response to DNA damage. Deletion of Exo1 in mice expressing a hypomorphic allele of Nbs1 leads to severe developmental impairment, embryonic death and chromosomal instability. While EXO1 plays a minimal role in normal cells, its loss strongly influences DNA replication, DNA repair, checkpoint signaling and damage sensitivity in NBS1 hypomorphic cells. Collectively, our results establish a key role for EXO1 in modulating the severity of hypomorphic MRE11 complex mutations.

Indexed as

DNA RepairEmbryonic DevelopmentAllelesAnimalsAtaxia Telangiectasia Mutated ProteinsCamptothecinCell Cycle ProteinsCells, CulturedChromosomal InstabilityDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA Repair EnzymesDNA ReplicationExodeoxyribonucleasesG2 Phase Cell Cycle CheckpointsGene DeletionAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseAtr protein, mouseCamptothecinCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesExo1 protein, mouseExodeoxyribonucleasesNijmegen breakage syndrome 1 protein, mouseNuclear Proteins

Identifiers

PMID26160886
PMCPMC4551929
OpenAlexW1916817328

What OpenQuestion holds

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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.