ArticleNature communications2018
A licensing step links AID to transcription elongation for mutagenesis in B cells.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 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
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- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- DNA secondary structures in BCL2 and MYC elicit activation-induced cytidine deaminase binding and activity.Nucleic acids research · 2026Article
- Somatic hypermutation patterns are shaped by both motif position and sequence grammar.The EMBO journal · 2026Article
- DOT1L activity limits transcription elongation velocity and favors RNAPII pausing to facilitate mutagenesis by AID.Nature communications · 2026Article
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.Molecular cell · 2025Article
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Epigenetic activation of JAG1 by AID contributes to metastasis of hepatocellular carcinoma.The Journal of biological chemistry · 2025Article
- Nucleotide level mapping of uracils in murine heavy chain switch regions shows correlation between uracilation and positions of switch junctions created during class-switch recombination.NAR molecular medicine · 2025Article
- The hGIDLife science alliance · 2024Article
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.bioRxiv : the preprint server for biology · 2024Article
- Conserved role of hnRNPL in alternative splicing of epigenetic modifiers enables B cell activation.EMBO reports · 2024Article
- APOBEC2 safeguards skeletal muscle cell fate through binding chromatin and regulating transcription of non-muscle genes during myoblast differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- The off-target effects of AID in carcinogenesis.Frontiers in immunology · 2023Review
- Pan-cancer landscape of AID-related mutations, composite mutations, and their potential role in the ICI response.NPJ precision oncology · 2022Article
- AFF3, a susceptibility factor for autoimmune diseases, is a molecular facilitator of immunoglobulin class switch recombination.Science advances · 2022Article
- C-terminal deletion-induced condensation sequesters AID from IgH targets in immunodeficiency.The EMBO journal · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
Abstract
Activation-induced deaminase (AID) mutates the immunoglobulin (Ig) genes to initiate somatic hypermutation (SHM) and class switch recombination (CSR) in B cells, thus underpinning antibody responses. AID mutates a few hundred other loci, but most AID-occupied genes are spared. The mechanisms underlying productive deamination versus non-productive AID targeting are unclear. Here we show that three clustered arginine residues define a functional AID domain required for SHM, CSR, and off-target activity in B cells without affecting AID deaminase activity or Escherichia coli mutagenesis. Both wt AID and mutants with single amino acid replacements in this domain broadly associate with Spt5 and chromatin and occupy the promoter of AID target genes. However, mutant AID fails to occupy the corresponding gene bodies and loses association with transcription elongation factors. Thus AID mutagenic activity is determined not by locus occupancy but by a licensing mechanism, which couples AID to transcription elongation.
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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.