ArticleThe Journal of experimental medicine2005
Intricate targeting of immunoglobulin somatic hypermutation maximizes the efficiency of affinity maturation.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- Trial
- Mutability and hypermutation antagonize immunoglobulin codon optimality.Molecular cell · 2025Article
- Review
- Efficient evolution of human antibodies from general protein language models.Nature biotechnology · 2024Article
- Article
- Avidity optimization of a MAGE-A1-specific TCR with somatic hypermutation.European journal of immunology · 2021Article
- Inferred Allelic Variants of Immunoglobulin Receptor Genes: A System for Their Evaluation, Documentation, and Naming.Frontiers in immunology · 2019Review
- What Are the Primary Limitations in B-Cell Affinity Maturation, and How Much Affinity Maturation Can We Drive with Vaccination? Is Affinity Maturation a Self-Defeating Process for Eliciting Broad Protection?Cold Spring Harbor perspectives in biology · 2018Review
- Beyond Hot Spots: Biases in Antibody Somatic Hypermutation and Implications for Vaccine Design.Frontiers in immunology · 2018Review
- Integrity of immunoglobulin variable regions is supported by GANP during AID-induced somatic hypermutation in germinal center B cells.International immunology · 2017Article
- Antibodyomics: bioinformatics technologies for understanding B-cell immunity to HIV-1.Immunological reviews · 2017Review
- Article
- Targeted AID-mediated mutagenesis (TAM) enables efficient genomic diversification in mammalian cells.Nature methods · 2016Article
- B Cell Responses during Secondary Dengue Virus Infection Are Dominated by Highly Cross-Reactive, Memory-Derived Plasmablasts.Journal of virology · 2016Article
- Effects of Darwinian Selection and Mutability on Rate of Broadly Neutralizing Antibody Evolution during HIV-1 Infection.PLoS computational biology · 2016Article
- BRILIA: Integrated Tool for High-Throughput Annotation and Lineage Tree Assembly of B-Cell Repertoires.Frontiers in immunology · 2016Article
- Assigning and visualizing germline genes in antibody repertoires.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Article
- The evolution within us.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Immunoglobulin VH gene diversity and somatic hypermutation during SIV infection of rhesus macaques.Immunogenetics · 2015Article
- Overlapping hotspots in CDRs are critical sites for V region diversification.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
It is believed that immunoglobulin-variable region gene (IgV) somatic hypermutation (SHM) is initiated by activation-induced cytidine deaminase (AID) upon deamination of cytidine to deoxyuracil. Patch-excision repair of these lesions involving error prone DNA polymerases such as poleta causes mutations at all base positions. If not repaired, the deaminated nucleotides on the coding and noncoding strands result in C-to-T and G-to-A exchanges, respectively. Herein it is reported that IgV gene evolution has been considerably influenced by the need to accommodate extensive C deaminations and the resulting accumulation of C-to-T and G-to-A exchanges. Although seemingly counterintuitive, the precise placement of C and G nucleotides causes most C-to-T and G-to-A mutations to be silent or conservative. We hypothesize that without intricate positioning of C and G nucleotides the efficiency of affinity maturation would be significantly reduced due to a dominance of replacements caused by C and G transition mutations. The complexity of these evolved biases in codon use are compounded by the precise concomitant hotspot/coldspot targeting of AID activity and Poleta errors to maximize SHM in the CDRs and minimize mutations in the FWRs.
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Identifiers
What OpenQuestion holds
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.