Evidence map›Paper›PMID 20368578›Full record

ArticleThe Journal of experimental medicine2010

53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination.

Anne Bothmer, Davide F Robbiani, Niklas Feldhahn, Anna Gazumyan, Andre Nussenzweig, Michel C Nussenzweig

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 276 citations in OpenAlex.

  1. Article
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  5. Review
  6. Review
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  8. Article
  9. A dual role of Cohesin in DNA DSB repair.Nature communications · 2025
    Article
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  11. Article
  12. Small Molecule MIF Modulation Enhances Ferroptosis by Impairing DNA Repair Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Efficient and sustainedMolecular therapy. Methods & clinical development · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Article

123 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

6 authors at 3 institutions in 1 country.

Anne BothmerLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Davide F Robbiani
Niklas Feldhahn
Anna Gazumyan
Andre Nussenzweig
Michel C Nussenzweig
Howard Hughes Medical Institute · USRockefeller University · USNational Cancer Institute · US

Funding

DNA RepairZIABC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Relationship between DNA damage detection and signalingZIABC010959 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
SIGNALLING PATHWAYS IN AUTOIMMUNITYR01AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 1994 to 2012
$5.0M
Howard Hughes Medical InstituteIntramural NIH HHSNIAID NIH HHS 1R0AI072529-01NIAID NIH HHS 5R01AI037526NIAID NIH HHS R01 AI037526
6 · The paper itself

Abstract

Class switch recombination (CSR) diversifies antibodies by joining highly repetitive DNA elements, which are separated by 60-200 kbp. CSR is initiated by activation-induced cytidine deaminase, an enzyme that produces multiple DNA double-strand breaks (DSBs) in switch regions. Switch regions are joined by a mechanism that requires an intact DNA damage response and classical or alternative nonhomologous end joining (A-NHEJ). Among the DNA damage response factors, 53BP1 has the most profound effect on CSR. We explore the role of 53BP1 in intrachromosomal DNA repair using I-SceI to introduce paired DSBs in the IgH locus. We find that the absence of 53BP1 results in an ataxia telangiectasia mutated-dependent increase in DNA end resection and that resected DNA is preferentially repaired by microhomology-mediated A-NHEJ. We propose that 53BP1 favors long-range CSR in part by protecting DNA ends against resection, which prevents A-NHEJ-dependent short-range rejoining of intra-switch region DSBs.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCell Cycle ProteinsChromosomal Proteins, Non-HistoneChromosome PairingCytidine DeaminaseDeoxyribonucleases, Type II Site-SpecificDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairImmunoglobulin Class SwitchingImmunoglobulin Heavy ChainsIntegrasesInterleukin-4AICDA (Activation-Induced Cytidine Deaminase)Ataxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsChromosomal Proteins, Non-HistoneCre recombinaseCytidine DeaminaseDeoxyribonucleases, Type II Site-SpecificDNA-Binding ProteinsImmunoglobulin Heavy ChainsIntegrasesInterleukin-4Intracellular Signaling Peptides and ProteinsLipopolysaccharidesProtein Serine-Threonine KinasesTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1Tumor Suppressor Proteins

Identifiers

PMID20368578
PMCPMC2856023
OpenAlexW2146507524

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.