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Article

Somatic Hypermutation and Class Switch Recombination in Msh6−/−Ung−/− Double-Knockout Mice

1 Oct 2006

Abstract excerpt

Somatic hypermutation (SHM) and class switch recombination (CSR) are initiated by activation-induced cytosine deaminase (AID). The uracil, and potentially neighboring bases, are processed by error-prone base excision repair and mismatch repair. Deficiencies in Ung, Msh2, or Msh6 affect SHM and CSR. To determine whether Msh2/Msh6 complexes which recognize single-base mismatches and loops were the only...

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PMID: 17015724
DOI: 10.4049/jimmunol.177.8.5386

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Related research

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Click a neighbor to travelStep 1 · 12 closest

Somatic Hypermutation and Class Switch Recombination in Msh6−/−Ung−/− Double-Knockout MicePMID 17015724Read ↗

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

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

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

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

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

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

Uracil excision by endogenous SMUG1 glycosylase promotes efficient Ig class switching and impacts on A:T substitutions during somatic mutation.Semantic proximity Read ↗

Mismatch recognition and uracil excision provide complementary paths to both Ig switching and the A/T-focused phase of somatic mutation.Semantic proximity Read ↗

The mismatch repair pathway functions normally at a non-AID target in germinal center B cells.Semantic proximity Read ↗

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