Evidence map›Paper›PMID 17606631›Full record

ArticleThe Journal of experimental medicine2007

Role for DNA repair factor XRCC4 in immunoglobulin class switch recombination.

Pauline Soulas-Sprauel, Gwenaël Le Guyader, Paola Rivera-Munoz, Vincent Abramowski, Christelle Olivier-Martin, Cécile Goujet-Zalc, Pierre Charneau, Jean-Pierre de Villartay

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Inborn errors of immunity caused by defects in the DNA damage response pathways: Importance of minimizing treatment-related genotoxicity.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2022
    Review
  9. Review
  10. DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Review
  13. Article
  14. AnThe Journal of biological chemistry · 2020
    Article
  15. Article
  16. DNA double-strand break response factors influence end-joining features of IgH class switch and general translocation junctions.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Physiological Roles of DNA Double-Strand Breaks.Journal of nucleic acids · 2017
    Review
  18. Redundant function of DNA ligase 1 and 3 in alternative end-joining during immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 1 country.

Pauline Soulas-SprauelInstitut National de la Santé et de la Recherche Médicale Unité 768, F-75015 Paris, France.
Gwenaël Le Guyader
Paola Rivera-Munoz
Vincent Abramowski
Christelle Olivier-Martin
Cécile Goujet-Zalc
Pierre Charneau
Jean-Pierre de Villartay
Délégation Paris 5 · FRInserm · FRCentre National de la Recherche Scientifique · FRInstitut Pasteur · FRTransgene (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

V(D)J recombination and immunoglobulin class switch recombination (CSR) are two somatic rearrangement mechanisms that proceed through the introduction of double-strand breaks (DSBs) in DNA. Although the DNA repair factor XRCC4 is essential for the resolution of DNA DSB during V(D)J recombination, its role in CSR has not been established. To bypass the embryonic lethality of XRCC4 deletion in mice, we developed a conditional XRCC4 knockout (KO) using LoxP-flanked XRCC4 cDNA lentiviral transgenesis. B lymphocyte restricted deletion of XRCC4 in these mice lead to an average two-fold reduction in CSR in vivo and in vitro. Our results connect XRCC4 and the nonhomologous end joining DNA repair pathway to CSR while reflecting the possible use of an alternative pathway in the repair of CSR DSB in the absence of XRCC4. In addition, this new conditional KO approach should be useful in studying other lethal mutations in mice.

Indexed as

DNA RepairImmunoglobulin Class SwitchingAnimalsB-LymphocytesDNA-Binding ProteinsGenes, LethalLentivirusMiceMice, KnockoutMice, TransgenicMutationDNA-Binding ProteinsXRCC4 protein, humanXRCC4 protein, mouse

Identifiers

PMID17606631
PMCPMC2118634
OpenAlexW2167368071

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.