ArticleThe Journal of experimental medicine2003
Mlh1 can function in antibody class switch recombination independently of Msh2.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 57 citations in OpenAlex.
- B cell class switch recombination is regulated by DYRK1A through MSH6 phosphorylation.Nature communications · 2023Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- MBD4 Facilitates Immunoglobulin Class Switch Recombination.Molecular and cellular biology · 2017Article
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.Advances in immunology · 2014Review
- AIDing antibody diversity by error-prone mismatch repair.Seminars in immunology · 2012Review
- Combinatorial mechanisms regulating AID-dependent DNA deamination: interacting proteins and post-translational modifications.Seminars in immunology · 2012Review
- Mismatch-mediated error prone repair at the immunoglobulin genes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2011Review
- Mismatch repair proteins MSH2, MLH1, and EXO1 are important for class-switch recombination events occurring in B cells that lack nonhomologous end joining.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- AID and somatic hypermutation.Advances in immunology · 2010Review
- Pol zeta ablation in B cells impairs the germinal center reaction, class switch recombination, DNA break repair, and genome stability.The Journal of experimental medicine · 2009Article
- Activities of human exonuclease 1 that promote cleavage of transcribed immunoglobulin switch regions.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Ubiquitylated PCNA plays a role in somatic hypermutation and class-switch recombination and is required for meiotic progression.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- DNA polymerase beta is able to repair breaks in switch regions and plays an inhibitory role during immunoglobulin class switch recombination.The Journal of experimental medicine · 2007Article
- DNA polymerase eta is the sole contributor of A/T modifications during immunoglobulin gene hypermutation in the mouse.The Journal of experimental medicine · 2007Article
- A role for the MutL mismatch repair Mlh3 protein in immunoglobulin class switch DNA recombination and somatic hypermutation.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Deletion of the nucleotide excision repair gene Ercc1 reduces immunoglobulin class switching and alters mutations near switch recombination junctions.The Journal of experimental medicine · 2004Article
- Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification.The Journal of experimental medicine · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mismatch repair proteins participate in antibody class switch recombination, although their roles are unknown. Previous nucleotide sequence analyses of switch recombination junctions indicated that the roles of Msh2 and the MutL homologues, Mlh1 and Pms2, differ. We now asked if Msh2 and Mlh1 function in the same pathway during switch recombination. Splenic B cells from mice deficient in both these proteins were induced to undergo switching in culture. The frequency of switching is reduced, similarly to that of B cells singly deficient in Msh2 or Mlh1. However, the nucleotide sequences of the Smu-Sgamma3 junctions resemble junctions from Mlh1- but not from Msh2-deficient cells, suggesting Mlh1 functions either independently of or before Msh2. The substitution mutations within S regions that are known to accompany switch recombination are increased in Msh2- and Mlh1 single-deficient cells and further increased in the double-deficient cells, again suggesting these proteins function independently in class switch recombination. The finding that MMR functions to reduce mutations in switch regions is unexpected since MMR proteins have been shown to contribute to somatic hypermutation of antibody variable region genes.
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Registered trials
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.