ArticleThe Journal of cell biology2004
53BP1 is required for class switch recombination.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers.
What it found
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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.
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.
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Who cites it
190 citing papers in PubMed, 320 citations in OpenAlex.
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- 53BP1 orchestrates sequence feature of RAG targets to balance DNA repair outcomes during V(D)J recombination.Science advances · 2026Article
- New twist on BRCA1-mediated DNA recombination repair and tumor suppression.Trends in cell biology · 2026Review
- 53BP1-RIF1 and DNA-PKcs show distinct genetic interactions with diverse chromosomal break repair outcomes.Nature communications · 2025Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).Nature communications · 2024Article
- SETD8 inhibition targets cancer cells with increased rates of ribosome biogenesis.Cell death & disease · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Article
- E3 ligases: a ubiquitous link between DNA repair, DNA replication and human disease.The Biochemical journal · 2024Review
- Endogenous p53 inhibitor TIRR dissociates systemic metabolic health from oncogenic activity.Cell reports · 2024Article
- The chromatin-associated 53BP1 ortholog, HSR-9, regulates recombinational repair andbioRxiv : the preprint server for biology · 2024Article
- IGH 3'RR recombination uncovers a non-germinal center imprint and c-MYC-dependent IGH rearrangement in unmutated chronic lymphocytic leukemia.Haematologica · 2024Article
- Mechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting.Nature communications · 2023Article
- ZEB1 promotes non-homologous end joining double-strand break repair.Nucleic acids research · 2023Article
- An AlphaFold2 map of the 53BP1 pathway identifies a direct SHLD3-RIF1 interaction critical for shieldin activity.EMBO reports · 2023Article
- DNA repair mechanisms that promote insertion-deletion events during immunoglobulin gene diversification.Science immunology · 2023Article
- Article
- Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination.eLife · 2022Article
- Review
- SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination.Nature communications · 2022Article
130 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
53BP1 participates early in the DNA damage response and is involved in cell cycle checkpoint control. Moreover, the phenotype of mice and cells deficient in 53BP1 suggests a defect in DNA repair (Ward et al., 2003b). Therefore, we asked whether or not 53BP1 would be required for the efficient repair of DNA double strand breaks. Our data indicate that homologous recombination by gene conversion does not depend on 53BP1. Moreover, 53BP1-deficient mice support normal V(D)J recombination, indicating that 53BP1 is not required for "classic" nonhomologous end joining. However, class switch recombination is severely impaired in the absence of 53BP1, suggesting that 53BP1 facilitates DNA end joining in a way that is not required or redundant for the efficient closing of RAG-induced strand breaks. These findings are similar to those observed in mice or cells deficient in the tumor suppressors ATM and H2AX, further suggesting that the functions of ATM, H2AX, and 53BP1 are closely linked.
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What OpenQuestion holds
Registered trials
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.