Evidence map›Paper›PMID 23576554›Full record

ArticleCancer research2013

Structure-specific endonucleases xpf and mus81 play overlapping but essential roles in DNA repair by homologous recombination.

Koji Kikuchi, Takeo Narita, Van T Pham, Junko Iijima, Kouji Hirota, Islam Shamima Keka, Mohiuddin, Katsuya Okawa, Tetsuya Hori, Tatsuo Fukagawa and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  10. Marine derivatives preventRoyal Society open science · 2021
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  16. SUMOylation of PCNA by PIAS1 and PIAS4 promotes template switch in the chicken and human B cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2018
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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

17 authors at 6 institutions in 4 countries.

Koji KikuchiDepartment of Radiation Genetics, and Frontier Technology Center, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Takeo Narita
Van T Pham
Junko Iijima
Kouji Hirota
Islam Shamima Keka
Mohiuddin
Katsuya Okawa
Tetsuya Hori
Tatsuo Fukagawa
Jeroen Essers
Roland Kanaar
Matthew C Whitby
Kaoru Sugasawa
Yoshihito Taniguchi
Katsumi Kitagawa
Shunichi Takeda
Nationwide Children's Hospital · USErasmus MC · NLNational Institute of Genetics · JPUniversity of Oxford · GBKobe University · JPKyoto University · JP

Funding

Kinetochore Function and Cell Cycle Progression RevisionR01GM068418 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KITAGAWA, KATSUMI · 2003 to 2012
$2.5M
Mechanisms of Mitotic Activation of the ATM kinaseR01CA133093 · NCI · SOUTHERN RESEARCH INSTITUTE · PI XU, BO · 2009 to 2013
$1.4M
NCI NIH HHS CA133093NCI NIH HHS R01 CA133093NIGMS NIH HHS GM68418NIGMS NIH HHS R01 GM068418Wellcome Trust
6 · The paper itself

Abstract

DNA double-strand breaks (DSB) occur frequently during replication in sister chromatids and are dramatically increased when cells are exposed to chemotherapeutic agents including camptothecin. Such DSBs are efficiently repaired specifically by homologous recombination (HR) with the intact sister chromatid. HR, therefore, plays pivotal roles in cellular proliferation and cellular tolerance to camptothecin. Mammalian cells carry several structure-specific endonucleases, such as Xpf-Ercc1 and Mus81-Eme1, in which Xpf and Mus81 are the essential subunits for enzymatic activity. Here, we show the functional overlap between Xpf and Mus81 by conditionally inactivating Xpf in the chicken DT40 cell line, which has no Mus81 ortholog. Although mammalian cells deficient in either Xpf or Mus81 are viable, Xpf inactivation in DT40 cells was lethal, resulting in a marked increase in the number of spontaneous chromosome breaks. Similarly, inactivation of both Xpf and Mus81 in human HeLa cells and murine embryonic stem cells caused numerous spontaneous chromosome breaks. Furthermore, the phenotype of Xpf-deficient DT40 cells was reversed by ectopic expression of human Mus81-Eme1 or human Xpf-Ercc1 heterodimers. These observations indicate the functional overlap of Xpf-Ercc1 and Mus81-Eme1 in the maintenance of genomic DNA. Both Mus81-Eme1 and Xpf-Ercc1 contribute to the completion of HR, as evidenced by the data that the expression of Mus81-Eme1 or Xpf-Ercc1 diminished the number of camptothecin-induced chromosome breaks in Xpf-deficient DT40 cells, and to preventing early steps in HR by deleting XRCC3 suppressed the nonviability of Xpf-deficient DT40 cells. In summary, Xpf and Mus81 have a substantially overlapping function in completion of HR.

Indexed as

DNA RepairHomologous RecombinationAnimalsCell DeathCell Line, TumorChickensChromosome AberrationsDNA-Binding ProteinsDNA Breaks, Double-StrandedEndonucleasesHeLa CellsHumansMiceDNA-Binding ProteinsEndonucleasesxeroderma pigmentosum group F protein

Identifiers

PMID23576554
PMCPMC3718858
OpenAlexW2126642086

What OpenQuestion holds

Textmetadata
LicenceTDM
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.