Evidence map›Paper›PMID 29511621›Full record

ArticleFEBS open bio2018

Robust DNA repair in PAXX-deficient mammalian cells.

Alisa Dewan, Mengtan Xing, Marie Benner Lundbæk, Raquel Gago-Fuentes, Carole Beck, Per Arne Aas, Nina-Beate Liabakk, Siri Sæterstad, Khac Thanh Phong Chau, Bodil Merete Kavli and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
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  8. DNA Damage Response.Biomolecules · 2021
    Article
  9. Article
  10. Review
  11. AnThe Journal of biological chemistry · 2020
    Article
  12. Article
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Alisa DewanDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Mengtan XingDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Marie Benner LundbækDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Raquel Gago-FuentesDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Carole BeckDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Per Arne AasDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Nina-Beate LiabakkDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Siri SæterstadDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Khac Thanh Phong ChauDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Bodil Merete KavliDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Valentyn OksenychDepartment of Clinical and Molecular Medicine (IKOM) Norwegian University of Science and Technology Trondheim Norway.
Norwegian University of Science and Technology · NOSt Olav's University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To ensure genome stability, mammalian cells employ several DNA repair pathways. Nonhomologous DNA end joining (NHEJ) is the DNA repair process that fixes double-strand breaks throughout the cell cycle. NHEJ is involved in the development of B and T lymphocytes through its function in V(D)J recombination and class switch recombination (CSR). NHEJ consists of several core and accessory factors, including Ku70, Ku80, XRCC4, DNA ligase 4, DNA-PKcs, Artemis, and XLF. Paralog of XRCC4 and XLF (PAXX) is the recently described accessory NHEJ factor that structurally resembles XRCC4 and XLF and interacts with Ku70/Ku80. To determine the physiological role of PAXX in mammalian cells, we purchased and characterized a set of custom-generated and commercially available NHEJ-deficient human haploid HAP1 cells,

Indexed as

CH12F3class switch recombinationetoposideHAP1IgAzeocin

Identifiers

PMID29511621
PMCPMC5832976
OpenAlexW2783951142

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.