Evidence map›Paper›PMID 27601299›Full record

ArticleCell reports2016

Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination.

Chloé Lescale, Hélène Lenden Hasse, Andrew N Blackford, Gabriel Balmus, Joy J Bianchi, Wei Yu, Léa Bacoccina, Angélique Jarade, Christophe Clouin, Rohan Sivapalan and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  6. Article
  7. Phosphorylation of DNA-PKcs at the S2056 cluster ensures efficient and productive lymphocyte development in XLF-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. The mechanisms of human lymphoid chromosomal translocations and their medical relevance.Critical reviews in biochemistry and molecular biology · 2022
    Article
  12. 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
  13. Review
  14. Article
  15. Review
  16. Review
  17. Assessing DNA Damage Responses Using B Lymphocyte Cultures.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  18. Article
  19. Review
  20. Article
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

13 authors at 6 institutions in 2 countries.

Chloé LescaleDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Hélène Lenden HasseDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Andrew N BlackfordWeatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK; CRUK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford OX3 7DQ, UK; The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
Gabriel BalmusThe Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Maintenance of Genome Stability, Genome Campus, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Joy J BianchiDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France; Cellule Pasteur, University of Paris René Descartes, Sorbonne Paris Cité, Paris 75015, France.
Wei YuDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Léa BacoccinaDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Angélique JaradeDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Christophe ClouinDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France.
Rohan SivapalanThe Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
Bernardo Reina-San-MartinInstitut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM-U964, CNRS-UMR7104, University of Strasbourg, 67400 Illkirch, France.
Stephen P JacksonThe Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Maintenance of Genome Stability, Genome Campus, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Ludovic DerianoDepartments of Immunology and Genomes and Genetics, Institut Pasteur, 75015 Paris, France. Electronic address: ludovic.deriano@pasteur.fr.
Institut Pasteur · FRWellcome Trust · GBCentre National de la Recherche Scientifique · FRJohn Radcliffe Hospital · GBSorbonne Paris Cité · FRUniversity of Cambridge · GB

Funding

Cancer Research UK 18796Cancer Research UK C6946/A14492Cancer Research UK C6/A18796European Research Council 310917Wellcome Trust WT092096
6 · The paper itself

Abstract

Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V(D)J recombination are masked by redundant joining activities. Thus, combined PAXX and XLF deficiency leads to an inability to join RAG-cleaved DNA ends. Additionally, we demonstrate that PAXX function in V(D)J recombination depends on its interaction with Ku. Importantly, we show that, unlike XLF, the role of PAXX during the repair of DNA breaks does not overlap with ATM and the RAG complex. Our findings illuminate the role of PAXX in V(D)J recombination and support a model in which PAXX and XLF function during NHEJ repair of DNA breaks, whereas XLF, the RAG complex, and the ATM-dependent DNA damage response promote end joining by stabilizing DNA ends.

Indexed as

Sequence Homology, Amino AcidAnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCRISPR-Cas SystemsDNA-Binding ProteinsDNA DamageDNA RepairDNA Repair EnzymesGene DeletionGene EditingGene Rearrangement, B-LymphocyteImmunoglobulinsKu AutoantigenModels, BiologicalOncogene Proteins v-ablAtaxia Telangiectasia Mutated ProteinsDNA-Binding ProteinsDNA Repair EnzymesIgKImmunoglobulinsKu AutoantigenOncogene Proteins v-ablDNA repairNHEJPAXXV(D)J recombinationXLFXRCC4

Identifiers

PMID27601299
PMCPMC5033762
OpenAlexW2511852522

What OpenQuestion holds

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Registered trials

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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.