ArticleProceedings of the National Academy of Sciences of the United States of America2010
Impaired induction of DNA lesions during immunoglobulin class-switch recombination in humans influences end-joining repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Disease-associated CTNNBL1 mutation impairs somatic hypermutation by decreasing nuclear AID.The Journal of clinical investigation · 2020Article
- Decreased somatic hypermutation induces an impaired peripheral B cell tolerance checkpoint.The Journal of clinical investigation · 2016Article
- Novel and recurrent AID mutations underlie prevalent autosomal recessive form of HIGM in consanguineous patients.Immunogenetics · 2016Article
- Elucidation of IgH 3' region regulatory role during class switch recombination via germline deletion.Nature communications · 2015Article
- An inherited immunoglobulin class-switch recombination deficiency associated with a defect in the INO80 chromatin remodeling complex.The Journal of allergy and clinical immunology · 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
- 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
- Uracil excision by endogenous SMUG1 glycosylase promotes efficient Ig class switching and impacts on A:T substitutions during somatic mutation.European journal of immunology · 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
- A regulatory role for the cohesin loader NIPBL in nonhomologous end joining during immunoglobulin class switch recombination.The Journal of experimental medicine · 2013Article
- Admixture mapping in lupus identifies multiple functional variants within IFIH1 associated with apoptosis, inflammation, and autoantibody production.PLoS genetics · 2013Article
- Immunoglobulin class-switch DNA recombination: induction, targeting and beyond.Nature reviews. Immunology · 2012Review
- Cernunnos influences human immunoglobulin class switch recombination and may be associated with B cell lymphomagenesis.The Journal of experimental medicine · 2012Article
- Activation-induced cytidine deaminase in antibody diversification and chromosome translocation.Advances in cancer research · 2012Review
- AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Complex regulation and function of activation-induced cytidine deaminase.Trends in immunology · 2011Review
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ig class-switch recombination (CSR) is a region-specific process that exchanges the constant Ig heavy-chain region and thus modifies an antibody's effector function. DNA lesions in switch (S) regions are induced by activation-induced cytidine deaminase (AID) and uracil-DNA glycosylase 2 (UNG2), subsequently processed to DNA breaks, and resolved by either the classical nonhomologous end-joining pathway or the alternative end-joining pathway (XRCC4/DNA ligase 4- and/or Ku70/Ku80-independent and prone to increased microhomology usage). We examined whether the induction of DNA lesions influences DNA end-joining during CSR by analyzing Sμ-Sα recombination junctions in various human Ig CSR defects of DNA lesion induction. We observed a progressive trend toward the usage of microhomology in Sμ-Sα recombination junctions from AID-heterozygous to AID-autosomal dominant to UNG2-deficient B lymphocytes. We thus hypothesize that impaired induction of DNA lesions in S regions during CSR leads to unusual end-processing of the DNA breaks, resulting in microhomology-mediated end-joining, which could be an indication for preferential processing by alternative end-joining rather than by classical nonhomologous end-joining.
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