ArticleProceedings of the National Academy of Sciences of the United States of America1998
Altered spectra of hypermutation in antibodies from mice deficient for the DNA mismatch repair protein PMS2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 105 citations in OpenAlex.
- Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation.Science China. Life sciences · 2024Review
- DNA repair mechanisms that promote insertion-deletion events during immunoglobulin gene diversification.Science immunology · 2023Article
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Genomic uracil homeostasis during normal B cell maturation and loss of this balance during B cell cancer development.Molecular and cellular biology · 2014Article
- Does DNA repair occur during somatic hypermutation?Seminars in immunology · 2012Review
- DNA polymerase ζ generates tandem mutations in immunoglobulin variable regions.The Journal of experimental medicine · 2012Article
- Error-prone DNA repair activity during somatic hypermutation in shark B lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Controlling somatic hypermutation in immunoglobulin variable and switch regions.Immunologic research · 2010Review
- AID and somatic hypermutation.Advances in immunology · 2010Review
- Immunoglobulin class switch recombination: study through human natural mutants.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Article
- Hijacked DNA repair proteins and unchained DNA polymerases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Transcriptional pausing and stalling causes multiple clustered mutations by human activation-induced deaminase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Nucleotide excision repair in an immunoglobulin variable gene is less efficient than in a housekeeping gene.Molecular immunology · 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
- MSH2-MSH6 stimulates DNA polymerase eta, suggesting a role for A:T mutations in antibody genes.The Journal of experimental medicine · 2005Article
- Immunoglobulin class switch recombination is impaired in Atm-deficient mice.The Journal of experimental medicine · 2004Article
- Absence of DNA polymerase eta reveals targeting of C mutations on the nontranscribed strand in immunoglobulin switch regions.The Journal of experimental medicine · 2004Article
- Review
- Msh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombination.The Journal of experimental medicine · 2003Article
- H2AX is required for recombination between immunoglobulin switch regions but not for intra-switch region recombination or somatic hypermutation.The Journal of experimental medicine · 2003Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Mutations are introduced into rearranged Ig variable genes at a frequency of 10(-2) mutations per base pair by an unknown mechanism. Assuming that DNA repair pathways generate or remove mutations, the frequency and pattern of mutation will be different in variable genes from mice defective in repair. Therefore, hypermutation was studied in mice deficient for either the DNA nucleotide excision repair gene Xpa or the mismatch repair gene Pms2. High levels of mutation were found in variable genes from XPA-deficient and PMS2-deficient mice, indicating that neither nucleotide excision repair nor mismatch repair pathways generate hypermutation. However, variable genes from PMS2-deficient mice had significantly more adjacent base substitutions than genes from wild-type or XPA-deficient mice. By using a biochemical assay, we confirmed that tandem mispairs were repaired by wild-type cells but not by Pms2(-/-) human or murine cells. The data indicate that tandem substitutions are produced by the hypermutation mechanism and then processed by a PMS2-dependent pathway.
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