ArticleProceedings of the National Academy of Sciences of the United States of America2014
Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- Article
- Phase separation as an emerging regulatory framework in antibody class switching and genome stability.Frontiers in immunology · 2026Review
- TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events.Nature communications · 2024Article
- Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.MedComm · 2024Review
- A Novel Heterozygous Variant in AICDA Impairs Ig Class Switching and Somatic Hypermutation in Human B Cells and is Associated with Autosomal Dominant HIGM2 Syndrome.Journal of clinical immunology · 2024Article
- Modular cytosine base editing promotes epigenomic and genomic modifications.Nucleic acids research · 2024Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- C-terminal deletion-induced condensation sequesters AID from IgH targets in immunodeficiency.The EMBO journal · 2022Article
- AID function in somatic hypermutation and class switch recombination.Acta biochimica et biophysica Sinica · 2022Review
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- Current insights into the mechanism of mammalian immunoglobulin class switch recombination.Critical reviews in biochemistry and molecular biology · 2019Review
- Activation-induced deaminase and its splice variants associate with trisomy 12 in chronic lymphocytic leukemia.Annals of hematology · 2019Article
- AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice.Scientific reports · 2018Article
- Transient AID expression for in situ mutagenesis with improved cellular fitness.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
- RNA Exosome and Non-coding RNA-Coupled Mechanisms in AID-Mediated Genomic Alterations.Journal of molecular biology · 2017Review
- Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.Scientific reports · 2017Article
- Decreased somatic hypermutation induces an impaired peripheral B cell tolerance checkpoint.The Journal of clinical investigation · 2016Article
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 7 institutions in 4 countries.
Funding
Abstract
Activation-induced deaminase (AID) triggers antibody class switch recombination (CSR) in B cells by initiating DNA double strand breaks that are repaired by nonhomologous end-joining pathways. A role for AID at the repair step is unclear. We show that specific inactivation of the C-terminal AID domain encoded by exon 5 (E5) allows very efficient deamination of the AID target regions but greatly impacts the efficiency and quality of subsequent DNA repair. Specifically eliminating E5 not only precludes CSR but also, causes an atypical, enzymatic activity-dependent dominant-negative effect on CSR. Moreover, the E5 domain is required for the formation of AID-dependent Igh-cMyc chromosomal translocations. DNA breaks at the Igh switch regions induced by AID lacking E5 display defective end joining, failing to recruit DNA damage response factors and undergoing extensive end resection. These defects lead to nonproductive resolutions, such as rearrangements and homologous recombination that can antagonize CSR. Our results can explain the autosomal dominant inheritance of AID variants with truncated E5 in patients with hyper-IgM syndrome 2 and establish that AID, through the E5 domain, provides a link between DNA damage and repair during 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.