ArticleJournal of immunology (Baltimore, Md. : 1950)2011
AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- APE2 Promotes AID-Dependent Somatic Hypermutation in Primary B Cell Cultures That Is Suppressed by APE1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- C-terminal deletion-induced condensation sequesters AID from IgH targets in immunodeficiency.The EMBO journal · 2022Article
- The role of HIRA-dependent H3.3 deposition and its modifications in the somatic hypermutation of immunoglobulin variable regions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- AID Phosphorylation Regulates Mismatch Repair-Dependent Class Switch Recombination and Affinity Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- A Novel Regulator of Activation-Induced Cytidine Deaminase/APOBECs in Immunity and Cancer: Schrödinger's CATalytic Pocket.Frontiers in immunology · 2017Review
- Engineering and optimising deaminase fusions for genome editing.Nature communications · 2016Article
- UNG protects B cells from AID-induced telomere loss.The Journal of experimental medicine · 2016Article
- Activation-induced deoxycytidine deaminase (AID) co-transcriptional scanning at single-molecule resolution.Nature communications · 2015Article
- Nbs1 ChIP-Seq Identifies Off-Target DNA Double-Strand Breaks Induced by AID in Activated Splenic B Cells.PLoS genetics · 2015Article
- Overlapping hotspots in CDRs are critical sites for V region diversification.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
- AID/APOBEC deaminases and cancer.Oncoscience · 2015Review
- AID-initiated DNA lesions are differentially processed in distinct B cell populations.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 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
- ATM increases activation-induced cytidine deaminase activity at downstream S regions during class-switch recombination.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
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) is induced in B cells during an immune response and is essential for both class-switch recombination (CSR) and somatic hypermutation of Ab genes. The C-terminal 10 aa of AID are required for CSR but not for somatic hypermutation, although their role in CSR is unknown. Using retroviral transduction into mouse splenic B cells, we show that the C terminus is not required for switch (S) region double-strand breaks (DSBs) and therefore functions downstream of DSBs. Using chromatin immunoprecipitation, we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Sμ and Sγ3 regions, and this depends on the C terminus and the deaminase activity of AID. We also show that mismatch repair does not contribute to the efficiency of CSR in the absence of the AID C terminus. Although it has been demonstrated that both UNG and Msh2-Msh6 are important for introduction of S region DSBs, our data suggest that the ability of AID to recruit these proteins is important for DSB resolution, perhaps by directing the S region DSBs toward accurate and efficient CSR via nonhomologous end joining.
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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.