ArticleThe Journal of biological chemistry2008
Hypermutation at A/T sites during G.U mismatch repair in vitro by human B-cell lysates.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Immunoglobulin VH gene diversity and somatic hypermutation during SIV infection of rhesus macaques.Immunogenetics · 2015Article
- Immunoglobulin somatic hypermutation by APOBEC3/Rfv3 during retroviral infection.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Decreased mutation frequencies among immunoglobulin G variable region genes during viremic HIV-1 infection.PloS one · 2014Article
- Article
- Simultaneous in vitro characterisation of DNA deaminase function and associated DNA repair pathways.PloS one · 2013Article
- UNG shapes the specificity of AID-induced somatic hypermutation.The Journal of experimental medicine · 2012Article
- AID: a riddle wrapped in a mystery inside an enigma.Immunologic research · 2011Review
- Article
- Biochemical basis of immunological and retroviral responses to DNA-targeted cytosine deamination by activation-induced cytidine deaminase and APOBEC3G.The Journal of biological chemistry · 2009Review
- Interference of mismatch and base excision repair during the processing of adjacent U/G mispairs may play a key role in somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic hypermutation in the variable regions of immunoglobulin genes is required to produce high affinity antibody molecules. Somatic hypermutation results by processing G.U mismatches generated when activation-induced cytidine deaminase (AID) deaminates C to U. Mutations at C/G sites are targeted mainly at deamination sites, whereas mutations at A/T sites entail error-prone DNA gap repair. We used B-cell lysates to analyze salient features of somatic hypermutation with in vitro mutational assays. Tonsil and hypermutating Ramos B-cells convert C-->U in accord with AID motif specificities, whereas HeLa cells do not. Using tonsil cell lysates to repair a G.U mismatch, A/T and G/C targeted mutations occur about equally, whereas Ramos cell lysates make fewer mutations at A/T sites (approximately 24%) compared with G/C sites (approximately 76%). In contrast, mutations in HeLa cell lysates occur almost exclusively at G/C sites (> 95%). By recapitulating two basic features of B-cell-specific somatic hypermutation, G/C mutations targeted to AID hot spot motifs and elevated A/T mutations dependent on error-prone processing of G.U mispairs, these cell free assays provide a practical method to reconstitute error-prone mismatch repair using purified B-cell proteins.
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Registered trials
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