Evidence map›Paper›PMID 29511619›Full record

ArticleFEBS open bio2018

Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF.

Raquel Gago-Fuentes, Mengtan Xing, Siri Sæterstad, Antonio Sarno, Alisa Dewan, Carole Beck, Stefano Bradamante, Magnar Bjørås, Valentyn Oksenych

Open 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. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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, 39 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Review
  8. Article
  9. DNA Damage Response.Biomolecules · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. AnThe Journal of biological chemistry · 2020
    Article
  14. Article
  15. 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

9 authors at 3 institutions in 1 country.

Raquel Gago-FuentesInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Mengtan XingInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Siri SæterstadInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Antonio SarnoInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Alisa DewanInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Carole BeckInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Stefano BradamanteInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Magnar BjøråsInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Valentyn OksenychInstitute of Clinical and Molecular Medicine (IKOM) Laboratory Center Norwegian University of Science and Technology Trondheim Norway.
Norwegian University of Science and Technology · NOSt Olav's University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA repair consists of several cellular pathways which recognize and repair damaged DNA. The classical nonhomologous DNA end-joining (NHEJ) pathway repairs double-strand breaks in DNA. It is required for maturation of both B and T lymphocytes by supporting V(D)J recombination as well as B-cell differentiation during class switch recombination (CSR). Inactivation of NHEJ factors Ku70, Ku80, XRCC4, DNA ligase 4, DNA-PKcs, and Artemis impairs V(D)J recombination and blocks lymphocyte development. Paralogue of XRCC4 and XLF (PAXX) is an accessory NHEJ factor that has a significant impact on the repair of DNA lesions induced by ionizing radiation in human, murine, and chicken cells. However, the role of PAXX during development is poorly understood. To determine the physiological role of PAXX, we deleted part of the

Indexed as

C9orf142Cernunnoslymphocytemouse geneticsT‐FISHXLS

Identifiers

PMID29511619
PMCPMC5832975
OpenAlexW2783460793

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.