ArticleEuropean journal of immunology2014
Uracil excision by endogenous SMUG1 glycosylase promotes efficient Ig class switching and impacts on A:T substitutions during somatic mutation.
Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 40 citations in OpenAlex.
- What is in a name? Rethinking SMUG1 in genome maintenance.NAR cancer · 2025Review
- DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023Review
- Article
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- Nucleotide Pool Imbalance and Antibody Gene Diversification.Vaccines · 2021Review
- Review
- Intrinsic Strand-Incision Activity of Human UNG: Implications for Nick Generation in Immunoglobulin Gene Diversification.Frontiers in immunology · 2021Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- DNA Breaks in Ig V Regions Are Predominantly Single Stranded and Are Generated by UNG and MSH6 DNA Repair Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Excision of uracil from DNA by hSMUG1 includes strand incision and processing.Nucleic acids research · 2019Article
- Chicken MBD4 Regulates Immunoglobulin Diversification by Somatic Hypermutation.Frontiers in immunology · 2019Article
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- Uracil Accumulation and Mutagenesis Dominated by Cytosine Deamination in CpG Dinucleotides in Mice Lacking UNG and SMUG1.Scientific reports · 2017Article
- Integrity of immunoglobulin variable regions is supported by GANP during AID-induced somatic hypermutation in germinal center B cells.International immunology · 2017Article
- Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.Nucleic acids research · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Excision of uracil introduced into the immunoglobulin loci by AID is central to antibody diversification. While predominantly carried out by the UNG uracil-DNA glycosylase as reflected by deficiency in immunoglobulin class switching in Ung(-/-) mice, the deficiency is incomplete, as evidenced by the emergence of switched IgG in the serum of Ung(-/-) mice. Lack of switching in mice deficient in both UNG and MSH2 suggested that mismatch repair initiated a backup pathway. We now show that most of the residual class switching in Ung(-/-) mice depends upon the endogenous SMUG1 uracil-DNA glycosylase, with in vitro switching to IgG1 as well as serum IgG3, IgG2b, and IgA greatly diminished in Ung(-/-) Smug1(-/-) mice, and that Smug1 partially compensates for Ung deficiency over time. Nonetheless, using a highly MSH2-dependent mechanism, Ung(-/-) Smug1(-/-) mice can still produce detectable levels of switched isotypes, especially IgG1. While not affecting the pattern of base substitutions, SMUG1 deficiency in an Ung(-/-) background further reduces somatic hypermutation at A:T base pairs. Our data reveal an essential requirement for uracil excision in class switching and in facilitating noncanonical mismatch repair for the A:T phase of hypermutation presumably by creating nicks near the U:G lesion recognized by MSH2.
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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.