ArticleNature communications2014
A source of the single-stranded DNA substrate for activation-induced deaminase during somatic hypermutation.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 37 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
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- AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells.The Journal of experimental medicine · 2026Article
- DOT1L activity limits transcription elongation velocity and favors RNAPII pausing to facilitate mutagenesis by AID.Nature communications · 2026Article
- Modular cytosine base editing promotes epigenomic and genomic modifications.Nucleic acids research · 2024Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- 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
- A Bayesian model based computational analysis of the relationship between bisulfite accessible single-stranded DNA in chromatin and somatic hypermutation of immunoglobulin genes.PLoS computational biology · 2021Article
- Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- AID-RNA polymerase II transcription-dependent deamination of IgV DNA.Nucleic acids research · 2019Article
- Transient AID expression for in situ mutagenesis with improved cellular fitness.Scientific reports · 2018Article
- JMolecular immunology · 2018Article
- Human Immunodeficiency Virus Tat Protein Aids V Region Somatic Hypermutation in Human B Cells.mBio · 2018Article
- AICDA drives epigenetic heterogeneity and accelerates germinal center-derived lymphomagenesis.Nature communications · 2018Article
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- APOBEC3B cytidine deaminase targets the non-transcribed strand of tRNA genes in yeast.DNA repair · 2017Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
During somatic hypermutation (SHM), activation-induced deaminase (AID) mutates deoxycytidine on single-stranded DNA (ssDNA) generated by the transcription machinery, but the detailed mechanism remains unclear. Here we report a higher abundance of RNA polymerase II (Pol II) at the immunoglobulin heavy-chain variable (Igh-V) region compared with the constant region and partially transcribed Igh RNAs, suggesting a slower Pol II progression at Igh-V that could result in some early/premature transcription termination after prolonged pausing/stalling of Pol II. Knocking down RNA-exosome complexes, which could decrease premature transcription termination, leads to decreased SHM. Knocking down Spt5, which can augment premature transcription termination, leads to increase in both, SHM and the abundance of ssDNA substrates. Collectively, our data support the model that, following the reduction of Pol II progression (pausing or stalling) at the Igh-V, additional steps such as premature transcription termination are involved in providing ssDNA substrates for AID during SHM.
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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.