ArticleProceedings of the National Academy of Sciences of the United States of America2009
The C-terminal region of activation-induced cytidine deaminase is responsible for a recombination function other than DNA cleavage in class switch recombination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. 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, 62 citations in OpenAlex.
- AID self-assembly and multistranded DNA binding drive synapsis in class switch recombination.Nucleic acids research · 2026Article
- Insights on SNPs of Human Activation-Induced Cytidine Deaminase AID.International journal of molecular sciences · 2025Review
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Ago2 and a miRNA reduce Topoisomerase 1 for enhancing DNA cleavage in antibody diversification by activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Phf5a regulates DNA repair in class switch recombination via p400 and histone H2A variant deposition.The EMBO journal · 2021Article
- Lsh/HELLS is required for B lymphocyte development and immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Genetic regulation of antibody responsiveness to immunization in substrains of BALB/c mice.Immunology and cell biology · 2019Article
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- Functional requirements of AID's higher order structures and their interaction with RNA-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Individual substitution mutations in the AID C terminus that ablate IgH class switch recombination.PloS one · 2015Article
- IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- Opinion: uracil DNA glycosylase (UNG) plays distinct and non-canonical roles in somatic hypermutation and class switch recombination.International immunology · 2014Review
- Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Differential regulation of S-region hypermutation and class-switch recombination by noncanonical functions of uracil DNA glycosylase.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- C-terminal region of activation-induced cytidine deaminase (AID) is required for efficient class switch recombination and gene conversion.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Accumulation of the FACT complex, as well as histone H3.3, serves as a target marker for somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Scaffold functions of 14-3-3 adaptors in B cell immunoglobulin class switch DNA recombination.PloS one · 2013Article
- The histone chaperone Spt6 is required for activation-induced cytidine deaminase target determination through H3K4me3 regulation.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID) is an essential factor for the class switch recombination (CSR) and somatic hypermutation (SHM) of Ig genes. CSR and SHM are initiated by AID-induced DNA breaks in the S and V regions, respectively. Because truncation or frame-shift mutations at the carboxyl (C)-terminus of AID abolishes CSR but not SHM, the C-terminal region of AID likely is required for the targeting of DNA breaks in the S region. To test this hypothesis, we determined the precise location and relative amounts of AID-induced DNA cleavage using an in situ DNA end-labeling method. We established CH12F3-2 cell transfectants expressing the estrogen receptor (ER) fused with wild-type (WT) AID or a deletion mutant lacking the C-terminal 16 aa, JP8Bdel. We found that AID-ER, but not JP8Bdel-ER, caused a CSR to IgA from the addition of 4-hydroxy tamoxifen. In contrast, both WT AID and JP8Bdel induced DNA breaks in both the V and S regions. In addition, JP8Bdel enhanced c-myc/IgH translocations. Our findings indicate that the C-terminal domain of AID is not required for S-region DNA breaks but is required for S-region recombination after DNA cleavage. Therefore, AID does not distinguish between the V and S regions for cleavage, but carries another function specific to 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.