ArticleJournal of immunology (Baltimore, Md. : 1950)2014
ATM increases activation-induced cytidine deaminase activity at downstream S regions during class-switch recombination.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Hyper-IgM and acquired C1q complement deficiency in a patient withOxford medical case reports · 2023Article
- Loop extrusion promotes an alternate pathway for isotype switching.Cell reports · 2021Article
- Compartments and Connections Within the Germinal Center.Frontiers in immunology · 2021Review
- V(D)J recombination, somatic hypermutation and class switch recombination of immunoglobulins: mechanism and regulation.Immunology · 2020Review
- Novel specialized cell state and spatial compartments within the germinal center.Nature immunology · 2020Article
- At the intersection of DNA damage and immune responses.Nature reviews. Immunology · 2019Review
- A novel ATM mutation associated with elevated atypical lymphocyte populations, hyper-IgM, and cutaneous granulomas.Clinical immunology (Orlando, Fla.) · 2019Article
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- The Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- A Damage-Independent Role for 53BP1 that Impacts Break Order and Igh Architecture during Class Switch Recombination.Cell reports · 2016Article
- Nbs1 ChIP-Seq Identifies Off-Target DNA Double-Strand Breaks Induced by AID in Activated Splenic B Cells.PLoS genetics · 2015Article
- 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
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) initiates Ab class-switch recombination (CSR) in activated B cells resulting in exchanging the IgH C region and improved Ab effector function. During CSR, AID instigates DNA double-strand break (DSB) formation in switch (S) regions located upstream of C region genes. DSBs are necessary for CSR, but improper regulation of DSBs can lead to chromosomal translocations that can result in B cell lymphoma. The protein kinase ataxia telangiectasia mutated (ATM) is an important proximal regulator of the DNA damage response (DDR), and translocations involving S regions are increased in its absence. ATM phosphorylates H2AX, which recruits other DNA damage response (DDR) proteins, including mediator of DNA damage checkpoint 1 (Mdc1) and p53 binding protein 1 (53BP1), to sites of DNA damage. As these DDR proteins all function to promote repair and recombination of DSBs during CSR, we examined whether mouse splenic B cells deficient in these proteins would show alterations in S region DSBs when undergoing CSR. We find that in atm(-/-) cells Sμ DSBs are increased, whereas DSBs in downstream Sγ regions are decreased. We also find that mutations in the unrearranged Sγ3 segment are reduced in atm(-/-) cells. Our data suggest that ATM increases AID targeting and activity at downstream acceptor S regions during CSR and that in atm(-/-) cells Sμ DSBs accumulate as they lack a recombination partner.
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