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Article

B cells from hyper-IgM patients carrying UNG mutations lack ability to remove uracil from ssDNA and have elevated genomic uracil.

The Journal of experimental medicine - 20 Jun 2005

Kavli Bodil, Andersen Sonja, Otterlei Marit, Liabakk Nina B, Imai Kohsuke, Fischer Alain, Durandy Anne, Krokan Hans E, Slupphaug Geir

Abstract excerpt

The generation of high-affinity antibodies requires somatic hypermutation (SHM) and class switch recombination (CSR) at the immunoglobulin (Ig) locus. Both processes are triggered by activation-induced cytidine deaminase (AID) and require UNG-encoded uracil-DNA glycosylase. AID has been suggested to function as an mRNA editing deaminase or as a single-strand DNA deaminase. In the latter model, SHM may result from...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 15967827
DOI: 10.1084/jem.20050042
PMCID: PMC2212036

Genes

UNG
SMUG1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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B cells from hyper-IgM patients carrying UNG mutations lack ability to remove uracil from ssDNA and have elevated genomic uracil.PMID 15967827Read ↗

Further evidence for involvement of a noncanonical function of uracil DNA glycosylase in class switch recombination.Semantic proximity Read ↗

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SMUG1 is able to excise uracil from immunoglobulin genes: insight into mutation versus repair.Semantic proximity Read ↗

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Uracil–DNA glycosylase UNG1 isoform variant supports class switch recombination and repairs nuclear genomic uracilSemantic proximity Read ↗

Pms2 and uracil-DNA glycosylases act jointly in the mismatch repair pathway to generate Ig gene mutations at A-T base pairs.Semantic proximity Read ↗

UNG shapes the specificity of AID-induced somatic hypermutation.Semantic proximity Read ↗

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