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Article

A Role for Msh6 But Not Msh3 in Somatic Hypermutation and Class Switch Recombination

5 Jul 2004

Abstract excerpt

Somatic hypermutation is initiated by activation-induced cytidine deaminase (AID), and occurs in several kilobases of DNA around rearranged immunoglobulin variable (V) genes and switch (S) sites before constant genes. AID deaminates cytosine to uracil, which can produce mutations of C:G nucleotide pairs, and the mismatch repair protein Msh2 participates in generating substitutions of downstream A:T pairs. Msh2 is...

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PMID: 15238605
DOI: 10.1084/jem.20040691

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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A Role for Msh6 But Not Msh3 in Somatic Hypermutation and Class Switch RecombinationPMID 15238605Read ↗

Somatic Hypermutation and Class Switch Recombination in Msh6−/−Ung−/− Double-Knockout MiceSemantic proximity Read ↗

Examination of Msh6- and Msh3-deficient Mice in Class Switching Reveals Overlapping and Distinct Roles of MutS Homologues in Antibody DiversificationSemantic proximity Read ↗

The mismatch repair protein Msh6 influences the in vivo AID targeting to the Ig locus.Semantic proximity Read ↗

MSH2–MSH6 stimulates DNA polymerase η, suggesting a role for A:T mutations in antibody genesSemantic proximity Read ↗

Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern.Semantic proximity Read ↗

MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sites.Semantic proximity Read ↗

Mlh1 Can Function in Antibody Class Switch Recombination Independently of Msh2Semantic proximity Read ↗

Msh2 ATPase Activity Is Essential for Somatic Hypermutation at A-T Basepairs and for Efficient Class Switch RecombinationSemantic proximity Read ↗

The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2-/- ung-/- mice.Semantic proximity Read ↗

Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Semantic proximity Read ↗

Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium.Semantic proximity Read ↗

Role for Msh5 in the regulation of Ig class switch recombination.Semantic proximity Read ↗

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