Evidence map›Paper›PMID 24145515›Full record

ArticleThe Journal of experimental medicine2013

A regulatory role for the cohesin loader NIPBL in nonhomologous end joining during immunoglobulin class switch recombination.

Elin Enervald, Likun Du, Torkild Visnes, Andrea Björkman, Emma Lindgren, Josephine Wincent, Guntram Borck, Laurence Colleaux, Valerie Cormier-Daire, Dik C van Gent and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 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
2.5field-weighted citation impact, top 10% 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, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. A dual role of Cohesin in DNA DSB repair.Nature communications · 2025
    Article
  4. Orientation Regulation of Class-switch Recombination in Human B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Aberrant recombination and repair during immunoglobulin class switching in BRCA1-deficient human B cells.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. ATAD5 deficiency decreases B cell division and Igh recombination.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  19. Review
  20. IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Review
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

20 authors at 8 institutions in 7 countries.

Elin EnervaldDepartment of Cell and Molecular Biology, 2 Department of Laboratory Medicine, 3 Department of Molecular Medicine and Surgery, Karolinska Institutet, 171 77 Stockholm, Sweden.
Likun Du
Torkild Visnes
Andrea Björkman
Emma Lindgren
Josephine Wincent
Guntram Borck
Laurence Colleaux
Valerie Cormier-Daire
Dik C van Gent
Juan Pie
Beatriz Puisac
Noel Fcc de Miranda
Sven Kracker
Lennart Hammarström
Jean-Pierre de Villartay
Anne Durandy
Jacqueline Schoumans
Lena Ström
Qiang Pan-Hammarström
Institute of Molecular and Cell Biology · RUKarolinska Institutet · SEInserm · FRHôpital Necker-Enfants Malades · FRUniversidad de Zaragoza · ESCancer Genomics Centre · NLDélégation Paris 5 · FRUniversity Hospital of Lausanne · CH

Funding

European Research Council 242551
6 · The paper itself

Abstract

DNA double strand breaks (DSBs) are mainly repaired via homologous recombination (HR) or nonhomologous end joining (NHEJ). These breaks pose severe threats to genome integrity but can also be necessary intermediates of normal cellular processes such as immunoglobulin class switch recombination (CSR). During CSR, DSBs are produced in the G1 phase of the cell cycle and are repaired by the classical NHEJ machinery. By studying B lymphocytes derived from patients with Cornelia de Lange Syndrome, we observed a strong correlation between heterozygous loss-of-function mutations in the gene encoding the cohesin loading protein NIPBL and a shift toward the use of an alternative, microhomology-based end joining during CSR. Furthermore, the early recruitment of 53BP1 to DSBs was reduced in the NIPBL-deficient patient cells. Association of NIPBL deficiency and impaired NHEJ was also observed in a plasmid-based end-joining assay and a yeast model system. Our results suggest that NIPBL plays an important and evolutionarily conserved role in NHEJ, in addition to its canonical function in sister chromatid cohesion and its recently suggested function in HR.

Indexed as

DNA End-Joining RepairImmunoglobulin Class SwitchingAdolescentBase SequenceB-LymphocytesCase-Control StudiesCell Cycle ProteinsCell LineChildChild, PreschoolChromosomal Proteins, Non-HistoneCohesinsDe Lange SyndromeDNADNA Breaks, Double-StrandedHeterozygoteCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNAIntracellular Signaling Peptides and ProteinsNIPBL protein, humanProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID24145515
PMCPMC3832922
OpenAlexW2169728037

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.