ArticleNature immunology2010
Widespread genomic breaks generated by activation-induced cytidine deaminase are prevented by homologous recombination.
Article in Nature immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 99 citations in OpenAlex.
- AID induces intraclonal diversity and genomic damage in CD86(+) chronic lymphocytic leukemia cells.European journal of immunology · 2014Trial
- Adenine base editors induce off-target structure variations in mouse embryos and primary human T cells.Genome biology · 2024Article
- Engineering of cytosine base editors with DNA damage minimization and editing scope diversification.Nucleic acids research · 2023Article
- A new wave of innovations within the DNA damage response.Signal transduction and targeted therapy · 2023Review
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- SETD2 Haploinsufficiency Enhances Germinal Center-Associated AICDA Somatic Hypermutation to Drive B-cell Lymphomagenesis.Cancer discovery · 2022Article
- POGZ promotes homology-directed DNA repair in an HP1-dependent manner.EMBO reports · 2022Article
- Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Journal of clinical immunology · 2022Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- 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
- Article
- Enhancing the efficacy of glycolytic blockade in cancer cellsCancer biology & therapy · 2019Article
- AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice.Scientific reports · 2018Article
- Main steps in DNA double-strand break repair: an introduction to homologous recombination and related processes.Chromosoma · 2018Review
- A licensing step links AID to transcription elongation for mutagenesis in B cells.Nature communications · 2018Article
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- Article
- Phosphorylation promotes activation-induced cytidine deaminase activity at the Myc oncogene.The Journal of experimental medicine · 2017Article
10 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
10 authors at 1 institution in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin class switching in activated B cells. Because AID has no known target-site specificity, there have been efforts to identify non-immunoglobulin AID targets. We show here that AID acts promiscuously, generating widespread DNA double-strand breaks (DSBs), genomic instability and cytotoxicity in B cells with less homologous recombination ability. We demonstrate that the homologous-recombination factor XRCC2 suppressed AID-induced off-target DSBs, promoting B cell survival. Finally, we suggest that aberrations that affect human chromosome 7q36, including XRCC2, correlate with genomic instability in B cell cancers. Our findings demonstrate that AID has promiscuous genomic DSB-inducing activity, identify homologous recombination as a safeguard against off-target AID action, and have implications for genomic instability in B cell cancers.
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.