ArticleThe Journal of experimental medicine2000
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.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 197 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
- UNG-RPA interaction governs the choice between high-fidelity and mutagenic uracil repair.Nucleic acids research · 2026Article
- FAM72A promotes UNG2 degradation and mutagenesis in human cancer cells.Scientific reports · 2025Article
- FAM72A degrades UNG2 through the GID/CTLH complex to promote mutagenic repair during antibody maturation.Nature communications · 2024Article
- DNA repair mechanisms that promote insertion-deletion events during immunoglobulin gene diversification.Science immunology · 2023Article
- B cell class switch recombination is regulated by DYRK1A through MSH6 phosphorylation.Nature communications · 2023Article
- Promoter Proximity Defines Mutation Window for VJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- Position-Dependent Differential Targeting of Somatic Hypermutation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- SHLD2 promotes class switch recombination by preventing inactivating deletions within the Igh locus.EMBO reports · 2020Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- What Targets Somatic Hypermutation to the Immunoglobulin Loci?Viral immunology · 2020Review
- 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 Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- Incomplete Segregation of MSH6 Frameshift Variants with Phenotype of Lynch Syndrome.International journal of molecular sciences · 2017Article
- Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.Nucleic acids research · 2017Article
- Targeted exome sequencing reveals distinct pathogenic variants in Iranians with colorectal cancer.Oncotarget · 2017Article
- DNA polymerase ι functions in the generation of tandem mutations during somatic hypermutation of antibody genes.The Journal of experimental medicine · 2016Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although the primary function of the DNA mismatch repair (MMR) system is to identify and correct base mismatches that have been erroneously introduced during DNA replication, recent studies have further implicated several MMR components in somatic hypermutation of immunoglobulin (Ig) genes. We studied the immune response in mice deficient in MutS homologue (MSH)3 and MSH6, two mutually exclusive partners of MSH2 that have not been examined previously for their role in Ig hypermutation. In Msh6(-)/- and Msh3(-)/-/Msh6(-)/- mice, base substitutions are preferentially targeted to G and C nucleotides and to an RGYW hot spot, as has been shown previously in Msh2(-)/- mice. In contrast, Msh3(-)/- mice show no differences from their littermate controls. These findings indicate that the MSH2-MSH6 heterodimer, but not the MSH2-MSH3 complex, is responsible for modulating Ig hypermutation.
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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.