Mismatch Recognition and Uracil Excision Provide Complementary Paths to Both Ig Switching and the A/T-Focused Phase of Somatic Mutation
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- 1 October 2004
- journal article
- research article
- Published by Elsevier in Molecular Cell
- Vol. 16 (2) , 163-171
- https://doi.org/10.1016/j.molcel.2004.10.011
Abstract
No abstract availableKeywords
This publication has 41 references indexed in Scilit:
- Uracil DNA Glycosylase Activity Is Dispensable for Immunoglobulin Class SwitchScience, 2004
- Replication protein A interacts with AID to promote deamination of somatic hypermutation targetsNature, 2004
- Comparison of the Differential Context-dependence of DNA Deamination by APOBEC Enzymes: Correlation with Mutation Spectra in VivoJournal of Molecular Biology, 2004
- Altered somatic hypermutation and reduced class-switch recombination in exonuclease 1–mutant miceNature Immunology, 2004
- AID Mediates Hypermutation by Deaminating Single Stranded DNAThe Journal of Experimental Medicine, 2003
- Transcription-targeted DNA deamination by the AID antibody diversification enzymeNature, 2003
- Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNaseProceedings of the National Academy of Sciences, 2003
- Altering the pathway of immunoglobulin hypermutation by inhibiting uracil-DNA glycosylaseNature, 2002
- Deficiency in Msh2 affects the efficiency and local sequence specificity of immunoglobulin class-switch recombination: parallels with somatic hypermutationThe EMBO Journal, 1999
- Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancerCell, 1995