ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Activation-induced cytidine deaminase-initiated off-target DNA breaks are detected and resolved during S phase.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- Tingible body macrophages arise from lymph node-resident precursors and uptake B cells by dendrites.The Journal of experimental medicine · 2023Article
- Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Journal of clinical immunology · 2022Article
- Abrogated AID Function Prolongs Survival and Diminishes Renal Pathology in the BXSB Mouse Model of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Non-canonical DNA/RNA structures during Transcription-Coupled Double-Strand Break Repair: Roadblocks or Bona fide repair intermediates?DNA repair · 2019Review
- Enhancing the efficacy of glycolytic blockade in cancer cellsCancer biology & therapy · 2019Article
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- Targeting mutagenesis in B cells: Phosphorylation goes beyond AID association.Molecular & cellular oncology · 2018Article
- Article
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- Defining ATM-Independent Functions of the Mre11 Complex with a Novel Mouse Model.Molecular cancer research : MCR · 2016Article
- Nbs1 ChIP-Seq Identifies Off-Target DNA Double-Strand Breaks Induced by AID in Activated Splenic B Cells.PLoS genetics · 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
- Checkpoint kinase 2 is required for efficient immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2014Article
- AIDing Chromatin and Transcription-Coupled Orchestration of Immunoglobulin Class-Switch Recombination.Frontiers in immunology · 2014Review
- Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.Advances in immunology · 2014Review
- A DNA break- and phosphorylation-dependent positive feedback loop promotes immunoglobulin class-switch recombination.Nature immunology · 2013Article
- Polyclonal hyper-IgE mouse model reveals mechanistic insights into antibody class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Attenuating homologous recombination stimulates an AID-induced antileukemic effect.The Journal of experimental medicine · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) initiates DNA double-strand breaks (DSBs) in the IgH gene (Igh) to stimulate isotype class switch recombination (CSR), and widespread breaks in non-Igh (off-target) loci throughout the genome. Because the DSBs that initiate class switching occur during the G₁ phase of the cell cycle, and are repaired via end joining, CSR is considered a predominantly G₁ reaction. By contrast, AID-induced non-Igh DSBs are repaired by homologous recombination. Although little is known about the connection between the cell cycle and either induction or resolution of AID-mediated non-Igh DSBs, their repair by homologous recombination implicates post-G₁ phases. Coordination of DNA breakage and repair during the cell cycle is critical to promote normal class switching and prevent genomic instability. To understand how AID-mediated events are regulated through the cell cycle, we have investigated G₁-to-S control in AID-dependent genome-wide DSBs. We find that AID-mediated off-target DSBs, like those induced in the Igh locus, are generated during G₁. These data suggest that AID-mediated DSBs can evade G₁/S checkpoint activation and persist beyond G₁, becoming resolved during S phase. Interestingly, DSB resolution during S phase can promote not only non-Igh break repair, but also Ig CSR. Our results reveal novel cell cycle dynamics in response to AID-initiated DSBs, and suggest that the regulation of the repair of these DSBs through the cell cycle may ensure proper class switching while preventing AID-induced genomic instability.
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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.