ArticleEuropean journal of immunology2014
Refining the Neuberger model: Uracil processing by activated B cells.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Know your enemy or find your friend?-Induction of IgA at mucosal surfaces.Immunological reviews · 2021Review
- Detection of Genomic Uracil Patterns.International journal of molecular sciences · 2021Review
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- Genome-wide alterations of uracil distribution patterns in human DNA upon chemotherapeutic treatments.eLife · 2020Article
- REV7 is required for processing AID initiated DNA lesions in activated B cells.Nature communications · 2020Article
- Large deletions in immunoglobulin genes are associated with a sustained absence of DNA Polymerase η.Scientific reports · 2020Article
- Clustered Mutations at the Murine and Human IgH Locus Exhibit Significant Linkage Consistent with Templated Mutagenesis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Positive Cofactor 4 (PC4) is critical for DNA repair pathway re-routing in DT40 cells.Scientific reports · 2016Article
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Topoisomerase I deficiency causes RNA polymerase II accumulation and increases AID abundance in immunoglobulin variable genes.DNA repair · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
During the immune response, B cells undergo a programed mutagenic cascade to promote increased affinity and expanded antibody function. The two processes, somatic hypermutation (SHM) and class switch recombination (CSR), are initiated by the protein activation-induced deaminase (AID), which converts cytosine to uracil in the immunoglobulin loci. The presence of uracil in DNA promotes DNA mutagenesis though a subset of DNA repair proteins. Two distinct mechanisms have been proposed to control uracil processing. The first is through base removal by uracil DNA glycosylase (UNG), and the second is through detection by the mismatch repair (MMR) complex MSH2/6. In a study published in this issue of European Journal of Immunology, Dingler et al. [Eur. J. Immunol. 2014. 44: 1925-1935] examine uracil processing in B cells in the absence of UNG and SMUG1 glycosylases. Similar to UNG, SMUG1 is an uracil glycosylase which can remove the uracil base. While Smug1(-/-) mice show no clear deficiency in SHM or CSR, Ung(-/-) Smug1(-/-) mice display exacerbated phenotypes, suggesting a back-up role for SMUG1 in antibody diversity. This new information expands the model of uracil processing in B cells and raises several interesting questions about the dynamic relationship between base excision repair and MMR.
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