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Article

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

PloS one - 17 Jun 2010

Roa Sergio, Li Ziqiang, Peled Jonathan U, Zhao Chunfang, Edelmann Winfried, Scharff Matthew D

Abstract excerpt

Mismatch repair of AID-generated dU:G mispairs is critical for class switch recombination (CSR) and somatic hypermutation (SHM) in B cells. The generation of a previously unavailable Msh2(-/-)Msh6(-/-) mouse has for the first time allowed us to examine the impact of the complete loss of MutSalpha on lymphomagenesis, CSR and SHM. The onset of T cell lymphomas and the survival of Msh2(-/-)Msh6(-/-) and...

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Share to AICDA (Activation-Induced Cytidine Deaminase)
Share to Base Pair Mismatch

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 20567595
DOI: 10.1371/journal.pone.0011182
PMCID: PMC2887398

Genes

MSH2
MSH6

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.

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MSH2/MSH6 complex promotes error-free repair of AID-induced dU:G mispairs as well as error-prone hypermutation of A:T sites.PMID 20567595Read ↗

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Mutating for Good: DNA Damage Responses During Somatic HypermutationSemantic proximity Read ↗

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

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