ArticlePLoS biology2014
Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.
Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Human antibody heavy chain variable region exon interacts with the 3' regulatory region to form a stable somatic hypermutation center.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- A 3D genome atlas of human tonsil and the role of loop extrusion in B cell somatic hypermutation.Science (New York, N.Y.) · 2026Article
- Engineering B cells to treat and study human disease.Nature biotechnology · 2025Review
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- Lineage- and stage-specific activity of antigen receptor gene enhancers during lymphocyte development.Frontiers in epigenetics and epigenomics · 2024Review
- Interpretable deep learning reveals the role of an E-box motif in suppressing somatic hypermutation of AGCT motifs within human immunoglobulin variable regions.Frontiers in immunology · 2024Article
- Oncogenic Merkel Cell Polyomavirus T Antigen Truncating Mutations are Mediated by APOBEC3 Activity in Merkel Cell Carcinoma.Cancer research communications · 2022Article
- Contribution of rare mutational outcomes to broadly neutralizing antibodies.Acta biochimica et biophysica Sinica · 2022Review
- AID function in somatic hypermutation and class switch recombination.Acta biochimica et biophysica Sinica · 2022Review
- HMCES protects immunoglobulin genes specifically from deletions during somatic hypermutation.Genes & development · 2022Article
- Ig Enhancers Increase RNA Polymerase II Stalling at Somatic Hypermutation Target Sequences.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The role of HIRA-dependent H3.3 deposition and its modifications in the somatic hypermutation of immunoglobulin variable regions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- How Chaotic Is Genome Chaos?Cancers · 2021Review
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- Transcription factor binding at Ig enhancers is linked to somatic hypermutation targeting.European journal of immunology · 2020Article
- Correlations in Somatic Hypermutation Between Sites in IGHV Genes Can Be Explained by Interactions Between AID and/or Polη Hotspots.Frontiers in immunology · 2020Article
- A licensing step links AID to transcription elongation for mutagenesis in B cells.Nature communications · 2018Article
- Review
- A double-strand break can trigger immunoglobulin gene conversion.Nucleic acids research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Somatic hypermutation (SH) generates point mutations within rearranged immunoglobulin (Ig) genes of activated B cells, providing genetic diversity for the affinity maturation of antibodies. SH requires the activation-induced cytidine deaminase (AID) protein and transcription of the mutation target sequence, but how the Ig gene specificity of mutations is achieved has remained elusive. We show here using a sensitive and carefully controlled assay that the Ig enhancers strongly activate SH in neighboring genes even though their stimulation of transcription is negligible. Mutations in certain E-box, NFκB, MEF2, or Ets family binding sites--known to be important for the transcriptional role of Ig enhancers--impair or abolish the activity. Full activation of SH typically requires a combination of multiple Ig enhancer and enhancer-like elements. The mechanism is evolutionarily conserved, as mammalian Ig lambda and Ig heavy chain intron enhancers efficiently stimulate hypermutation in chicken cells. Our results demonstrate a novel regulatory function for Ig enhancers, indicating that they either recruit AID or alter the accessibility of the nearby transcription units.
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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.