ArticleThe Journal of experimental medicine1998
A hypermutable insert in an immunoglobulin transgene contains hotspots of somatic mutation and sequences predicting highly stable structures in the RNA transcript.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 56 citations in OpenAlex.
- Interplay between Target Sequences and Repair Pathways Determines Distinct Outcomes of AID-Initiated Lesions.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- Multiple transcription factor binding sites predict AID targeting in non-Ig genes.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- The role of activation-induced deaminase in antibody diversification and genomic instability.Immunologic research · 2013Review
- V-region mutation in vitro, in vivo, and in silico reveal the importance of the enzymatic properties of AID and the sequence environment.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- 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
- Does antisense make sense of AID targeting?Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- AID to overcome the limitations of genomic information by introducing somatic DNA alterations.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2006Review
- Evaluation of molecular models for the affinity maturation of antibodies: roles of cytosine deamination by AID and DNA repair.Chemical reviews · 2006Review
- Variable deletion and duplication at recombination junction ends: implication for staggered double-strand cleavage in class-switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Quantitative regulation of class switch recombination by switch region transcription.The Journal of experimental medicine · 2001Article
- The translesion DNA polymerase zeta plays a major role in Ig and bcl-6 somatic hypermutation.Immunity · 2001Article
- Somatic hypermutation of immunoglobulin and non-immunoglobulin genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Transcription, beta-like DNA polymerases and hypermutation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Evolution and the molecular basis of somatic hypermutation of antigen receptor genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Hypermutation in bacteria and other cellular systems.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Different mismatch repair deficiencies all have the same effects on somatic hypermutation: intact primary mechanism accompanied by secondary modifications.The Journal of experimental medicine · 1999Article
- Hypermutation in derepressed operons of Escherichia coli K12.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Immunoglobulin (Ig) genes expressed in mature B lymphocytes can undergo somatic hypermutation upon cell interaction with antigen and T cells. The mutation mechanism had previously been shown to depend upon transcription initiation, suggesting that a mutator factor was loaded on an RNA polymerase initiating at the promoter and causing mutations during elongation (Peters, A., and U. Storb. 1996. Immunity. 4:57-65). To further elucidate this process we have created an artificial substrate consisting of alternating EcoRV and PvuII restriction enzyme sites (EPS) located within the variable (V) region of an Ig transgene. This substrate can easily be assayed for the presence of mutations in DNA from transgenic lymphocytes by amplifying the EPS insert and determining by restriction enzyme digestion whether any of the restriction sites have been altered. Surprisingly, the EPS insert was mutated many times more frequently than the flanking Ig sequences. In addition there were striking differences in mutability of the different nucleotides within the restriction sites. The data favor a model of somatic hypermutation where the fine specificity of the mutations is determined by nucleotide sequence preferences of a mutator factor, and where the general site of mutagenesis is determined by the pausing of the RNA polymerase due to secondary structures within the nascent RNA.
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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.