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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
Open accessAbstract
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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Citations
Cited by
DNA Mismatch Repair: Functions and Mechanisms
Iyer, R. R., Pluciennik, A., Burdett, V., & Modrich, P. L. (2006) · Chemical Reviews · doi:10.1021/cr0404794 · Cited by 905
Error-Prone Repair DNA Polymerases in Prokaryotes and Eukaryotes
Goodman, M. F. (2002) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.71.083101.124707 · Cited by 727
DNA‐damage repair; the good, the bad, and the ugly
Hakem, R. (2008) · The EMBO Journal · doi:10.1038/emboj.2008.15 · Cited by 549
AID Is Required for c-myc/IgH Chromosome Translocations In Vivo
Ramiro, A. R., Jankovic, M., Eisenreich, T., Difilippantonio, S., Chen-Kiang, S., Muramatsu, M., Honjo, T., Nussenzweig, A., & Nussenzweig, M. C. (2004) · Cell · doi:10.1016/j.cell.2004.08.006 · Cited by 465
The Biochemistry of Somatic Hypermutation
Peled, J. U., Kuang, F. L., Iglesias-Ussel, M. D., Roa, S., Kalis, S. L., Goodman, M. F., & Scharff, M. D. (2008) · Annual Review of Immunology · doi:10.1146/annurev.immunol.26.021607.090236 · Cited by 462
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Metadata
- Authors
- Wiesendanger, M., Kneitz, B., Edelmann, W., & Scharff, M. D.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2000-02-07
- Volume
- 191
- Issue
- 3
- Pages
- 579-584
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2166617268
- Cited by
- 195
- References
- 0
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: 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. https://app.cochat.ai/papers/10.1084/jem.191.3.579
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- Wiesendanger, M., Kneitz, B., Edelmann, W., & Scharff, M. D. (2000). 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. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.191.3.579
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