ArticleThe Journal of experimental medicine2013
Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switching.
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 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Recombination junctions from antibody isotype switching classify immune and DNA repair dysfunction.Nature communications · 2025Article
- Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection.Nature communications · 2025Article
- Testis-Specific Protein Y-Encoded (TSPY) Is Required for Male Early Embryo Development inInternational journal of molecular sciences · 2023Article
- Prognostic Significance of mRNA Expression RBBP8 or Its Methylation in Gliomas.Cellular and molecular neurobiology · 2023Article
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- Phosphorylation-dependent assembly of DNA damage response systems and the central roles of TOPBP1.DNA repair · 2021Review
- Multiple DSB Resection Activities Redundantly Promote Alternative End Joining-Mediated Class Switch Recombination.Frontiers in cell and developmental biology · 2021Article
- CtIP-mediated DNA resection is dispensable for IgH class switch recombination by alternative end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- 53BP1 Supports Immunoglobulin Class Switch Recombination Independently of Its DNA Double-Strand Break End Protection Function.Cell reports · 2019Article
- CtIP is essential for early B cell proliferation and development in mice.The Journal of experimental medicine · 2019Article
- 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 · 2018Article
- Phosphorylation promotes activation-induced cytidine deaminase activity at the Myc oncogene.The Journal of experimental medicine · 2017Article
- Article
- WRN regulates pathway choice between classical and alternative non-homologous end joining.Nature communications · 2016Article
- The DNA resection protein CtIP promotes mammary tumorigenesis.Oncotarget · 2016Article
- PREVENTING THE CHROMOSOMAL TRANSLOCATIONS THAT CAUSE CANCER.Transactions of the American Clinical and Climatological Association · 2016Article
- Ectopic expression of RNF168 and 53BP1 increases mutagenic but not physiological non-homologous end joining.Nucleic acids research · 2015Article
- Cyclin-dependent kinases regulate Ig class switching by controlling access of AID to the switch region.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- 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 · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 9 institutions in 1 country.
Funding
Abstract
DNA double-strand breaks (DSBs) are byproducts of normal cellular metabolism and obligate intermediates in antigen receptor diversification reactions. These lesions are potentially dangerous because they can lead to deletion of genetic material or chromosome translocation. The chromatin-binding protein 53BP1 and the histone variant H2AX are required for efficient class switch (CSR) and V(D)J recombination in part because they protect DNA ends from resection and thereby favor nonhomologous end joining (NHEJ). Here, we examine the mechanism of DNA end resection in primary B cells. We find that resection depends on both CtBP-interacting protein (CtIP, Rbbp8) and exonuclease 1 (Exo1). Inhibition of CtIP partially rescues the CSR defect in 53BP1- and H2AX-deficient lymphocytes, as does interference with the RecQ helicases Bloom (Blm) and Werner (Wrn). We conclude that CtIP, Exo1, and RecQ helicases contribute to the metabolism of DNA ends during DSB repair in B lymphocytes and that minimizing resection favors efficient CSR.
Indexed as
Identifiers
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.