ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2009
Non-homologous end joining in class switch recombination: the beginning of the end.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 61 citations in OpenAlex.
- Trial
- Defects in DNA damage signaling and cell cycle checkpoints in a mouse model of Rhno1 deletion.Cell death discovery · 2025Article
- Orientation Regulation of Class-switch Recombination in Human B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Current Strategies for Increasing Knock-In Efficiency in CRISPR/Cas9-Based Approaches.International journal of molecular sciences · 2024Review
- Antibody Repertoire Analysis of Tumor-Infiltrating B Cells Reveals Distinct Signatures and Distributions Across Tissues.Frontiers in immunology · 2021Article
- IL-23 Promotes a Coordinated B Cell Germinal Center Program for Class-Switch Recombination to IgG2b in BXD2 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Article
- Treatment May Be Harmful: Mechanisms/Prediction/Prevention of Drug-Induced DNA Damage and Repair in Multiple Myeloma.Frontiers in genetics · 2019Review
- DEK is required for homologous recombination repair of DNA breaks.Scientific reports · 2017Article
- AID/APOBEC-network reconstruction identifies pathways associated with survival in ovarian cancer.BMC genomics · 2016Article
- DCLRE1C (ARTEMIS) mutations causing phenotypes ranging from atypical severe combined immunodeficiency to mere antibody deficiency.Human molecular genetics · 2015Article
- APOBEC3B-Mediated Cytidine Deamination Is Required for Estrogen Receptor Action in Breast Cancer.Cell reports · 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
- Deregulation of DNA double-strand break repair in multiple myeloma: implications for genome stability.PloS one · 2015Article
- Human papillomavirus type 16 E7 oncoprotein causes a delay in repair of DNA damage.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2014Article
- IgA subclass switch recombination in human mucosal and systemic immune compartments.Mucosal immunology · 2014Article
- PP4 is essential for germinal center formation and class switch recombination in mice.PloS one · 2014Article
- DNA repair genes are selectively mutated in diffuse large B cell lymphomas.The Journal of experimental medicine · 2013Article
- Admixture mapping in lupus identifies multiple functional variants within IFIH1 associated with apoptosis, inflammation, and autoantibody production.PLoS genetics · 2013Article
- AIDing antibody diversity by error-prone mismatch repair.Seminars in immunology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin class switch recombination (CSR) is initiated by a B-cell-specific factor, activation-induced deaminase, probably through deamination of deoxycytidine residues within the switch (S) regions. The initial lesions in the S regions are subsequently processed, resulting in the production of DNA double-strand breaks (DSBs). These breaks will then be recognized, edited and repaired, finally leading to the recombination of the two S regions. Two major repair pathways have been implicated in CSR, the predominant non-homologous end joining (NHEJ) and the alternative end-joining (A-EJ) pathways. The former requires not only components of the 'classical' NHEJ machinery, i.e. Ku70/Ku80, DNA-dependent protein kinase catalytic subunit, DNA ligase IV and XRCC4, but also a number of DNA-damage sensors or adaptors, such as ataxia-telangiectasia mutated, gammaH2AX, 53BP1, MDC1, the Mre11-Rad50-NBS1 complex and the ataxia telangiectasia and Rad3-related protein (ATR). The latter pathway is not well characterized yet and probably requires microhomologies. In this review, we will focus on the current knowledge of the predominant NHEJ pathway in CSR and will also give a perspective on the A-EJ pathway.
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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.