ArticleMolecular immunology2008
I. VH gene transcription creates stabilized secondary structures for coordinated mutagenesis during somatic hypermutation.
Article in Molecular immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- Transcription-associated mutagenesis.Annual review of genetics · 2014Review
- Stabilised DNA secondary structures with increasing transcription localise hypermutable bases for somatic hypermutation in IGHV3-23.Immunogenetics · 2012Article
- Nonimmunoglobulin target loci of activation-induced cytidine deaminase (AID) share unique features with immunoglobulin genes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Gene Conversion-Like Events in the Diversification of Human Rearranged IGHV3-23*01 Gene Sequences.Frontiers in immunology · 2012Article
- Evolution of coordinated mutagenesis and somatic hypermutation in VH5.Molecular immunology · 2011Article
- Decrease in topoisomerase I is responsible for activation-induced cytidine deaminase (AID)-dependent somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Self-catalyzed site-specific depurination of G residues mediated by cruciform extrusion in closed circular DNA plasmids.The Journal of biological chemistry · 2011Article
- Altering the spectrum of immunoglobulin V gene somatic hypermutation by modifying the active site of AID.The Journal of experimental medicine · 2010Article
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During the adaptive immune response, antigen challenge triggers a million-fold increase in mutation rates in the variable-region antibody genes. The frequency of mutation is causally and directly linked to transcription, which provides ssDNA and drives supercoiling that stabilizes secondary structures containing unpaired, intrinsically mutable bases. Simulation analysis of transcription in VH5 reveals a dominant 65nt secondary structure in the non-transcribed strand containing six sites of mutable ssDNA that have also been identified independently in human B cell lines and in primary mouse B cells. This dominant structure inter-converts briefly with less stable structures and is formed repeatedly during transcription, due to periodic pauses and backtracking. In effect, this creates a stable yet dynamic "mutability platform" consisting of ever-changing patterns of unpaired bases that are simultaneously exposed and therefore able to coordinate mutagenesis. Such a complex of secondary structures may be the source of ssDNA for enzyme-based diversification, which ultimately results in high affinity antibodies.
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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.