ArticleThe Journal of experimental medicine2005
MSH2-MSH6 stimulates DNA polymerase eta, suggesting a role for A:T mutations in antibody genes.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
91 citing papers in PubMed, 191 citations in OpenAlex.
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- Deaminase-Driven Reverse Transcription Mutagenesis in Oncogenesis: Critical Analysis of Transcriptional Strand Asymmetries of Single Base Substitution Signatures.International journal of molecular sciences · 2025Review
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- Ataxia Telangiectasia Mutated and MSH2 Control Blunt DNA End Joining in Ig Class Switch Recombination.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- IRF4 deficiency vulnerates B-cell progeny for leukemogenesis via somatically acquired Jak3 mutations conferring IL-7 hypersensitivity.Cell death and differentiation · 2022Article
- A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus-like Disease in Mice.ACR open rheumatology · 2022Article
- Diverse mutational landscapes in human lymphocytes.Nature · 2022Article
- In crystallo observation of three metal ion promoted DNA polymerase misincorporation.Nature communications · 2022Article
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- SHLD2 promotes class switch recombination by preventing inactivating deletions within the Igh locus.EMBO reports · 2020Article
- Review
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- Multifaceted activities of DNA polymerase η: beyond translesion DNA synthesis.Current genetics · 2019Review
- DNA Breaks in Ig V Regions Are Predominantly Single Stranded and Are Generated by UNG and MSH6 DNA Repair Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The Camel Adaptive Immune Receptors Repertoire as a Singular Example of Structural and Functional Genomics.Frontiers in genetics · 2019Review
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- The Bayesian optimist's guide to adaptive immune receptor repertoire analysis.Immunological reviews · 2018Review
31 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Activation-induced cytidine deaminase deaminates cytosine to uracil (dU) in DNA, which leads to mutations at C:G basepairs in immunoglobulin genes during somatic hypermutation. The mechanism that generates mutations at A:T basepairs, however, remains unclear. It appears to require the MSH2-MSH6 mismatch repair heterodimer and DNA polymerase (pol) eta, as mutations of A:T are decreased in mice and humans lacking these proteins. Here, we demonstrate that these proteins interact physically and functionally. First, we show that MSH2-MSH6 binds to a U:G mismatch but not to other DNA intermediates produced during base excision repair of dUs, including an abasic site and a deoxyribose phosphate group. Second, MSH2 binds to pol eta in solution, and endogenous MSH2 associates with the pol in cell extracts. Third, MSH2-MSH6 stimulates the catalytic activity of pol eta in vitro. These observations suggest that the interaction between MSH2-MSH6 and DNA pol eta stimulates synthesis of mutations at bases located downstream of the initial dU lesion, including A:T pairs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.