Evidence map›Paper›PMID 25879486›Full record

ArticleNature communications2015

The DNA repair endonuclease Mus81 facilitates fast DNA replication in the absence of exogenous damage.

Haiqing Fu, Melvenia M Martin, Marie Regairaz, Liang Huang, Yang You, Chi-Mei Lin, Michael Ryan, RyangGuk Kim, Tsutomu Shimura, Yves Pommier and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 68 citations in OpenAlex.

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  19. Germline Mutation inCancers · 2020
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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

11 authors at 3 institutions in 2 countries.

Haiqing FuDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Melvenia M MartinDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Marie RegairazDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Liang HuangDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.ORCID http://orcid.org/0000-0003-1663-7025
Yang YouDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Chi-Mei LinDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Michael RyanInSilico Solutions, 11781 Lee Jackson Highway, Fairfax, Virginia 22033, USA.
RyangGuk KimInSilico Solutions, 11781 Lee Jackson Highway, Fairfax, Virginia 22033, USA.
Tsutomu ShimuraDepartment of Environmental Health, National Institute of Public Health 2-3-6 Minami, Wako, Saitama 351-0197, Japan.
Yves PommierDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Mirit I AladjemDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
National Cancer Institute · USInsilicos (United States) · USNational Institute of Public Health · JP

Funding

Initiation of DNA Replication in Mammalian CellsZIABC010411 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ALADJEM, MIRIT · 2009 to 2025
$25.0M
Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC010411
6 · The paper itself

Abstract

The Mus81 endonuclease resolves recombination intermediates and mediates cellular responses to exogenous replicative stress. Here, we show that Mus81 also regulates the rate of DNA replication during normal growth by promoting replication fork progression while reducing the frequency of replication initiation events. In the absence of Mus81 endonuclease activity, DNA synthesis is slowed and replication initiation events are more frequent. In addition, Mus81-deficient cells fail to recover from exposure to low doses of replication inhibitors and cell viability is dependent on the XPF endonuclease. Despite an increase in replication initiation frequency, cells lacking Mus81 use the same pool of replication origins as Mus81-expressing cells. Therefore, decelerated DNA replication in Mus81-deficient cells does not initiate from cryptic or latent origins not used during normal growth. These results indicate that Mus81 plays a key role in determining the rate of DNA replication without activating a novel group of replication origins.

Indexed as

Cell CycleCell SurvivalComet AssayDNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationEndonucleasesGene Knockdown TechniquesGene Knockout TechniquesHCT116 CellsHumansDNA-Binding ProteinsEndonucleasesMUS81 protein, humanxeroderma pigmentosum group F protein

Identifiers

PMID25879486
PMCPMC4400873
OpenAlexW1977586435

What OpenQuestion holds

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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.