ArticleCell2011
The RNA exosome targets the AID cytidine deaminase to both strands of transcribed duplex DNA substrates.
Article in Cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 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.
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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
200 citing papers in PubMed, 311 citations in OpenAlex.
- Article
- Article
- Beyond the Classical View: Early Emergence of Class Switch Recombination-Associated Molecular Features During B-Cell Development in the Bone Marrow.International journal of molecular sciences · 2026Review
- Mechanisms of transcription termination across the coding and noncoding loci of the genome.Nature reviews. Molecular cell biology · 2026Review
- Review
- R-loop disruption triggers irreversible topoisomerase 1-DNA cleavage complex formation during AID-dependent IgH gene diversification.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- ERCC6L2 ensures repair fidelity for staggered-end DNA double-strand breaks.Nature communications · 2026Article
- Epigenetic-Genetic Coupling and Understanding the Molecular and Cellular Basis of Lamarckian Inheritance.International journal of molecular sciences · 2026Review
- 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
- DIS3 licenses B cells for plasma cell differentiation in humans.Cellular & molecular immunology · 2026Article
- Estrogen influences class-switched memory B cell frequency only in humans with two X chromosomes.The Journal of experimental medicine · 2025Article
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.Molecular cell · 2025Article
- Deaminase-Driven Reverse Transcription Mutagenesis in Oncogenesis: Critical Analysis of Transcriptional Strand Asymmetries of Single Base Substitution Signatures.International journal of molecular sciences · 2025Review
- 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
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.bioRxiv : the preprint server for biology · 2024Article
- Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging.Ageing research reviews · 2024Review
- RNA biogenesis and RNA metabolism factors as R-loop suppressors: a hidden role in genome integrity.Genes & development · 2024Review
- RNA 2'-O-methylation promotes persistent R-loop formation and AID-mediated IgH class switch recombination.BMC biology · 2024Article
140 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Activation-induced cytidine deaminase (AID) initiates immunoglobulin (Ig) heavy-chain (IgH) class switch recombination (CSR) and Ig variable region somatic hypermutation (SHM) in B lymphocytes by deaminating cytidines on template and nontemplate strands of transcribed DNA substrates. However, the mechanism of AID access to the template DNA strand, particularly when hybridized to a nascent RNA transcript, has been an enigma. We now implicate the RNA exosome, a cellular RNA-processing/degradation complex, in targeting AID to both DNA strands. In B lineage cells activated for CSR, the RNA exosome associates with AID, accumulates on IgH switch regions in an AID-dependent fashion, and is required for optimal CSR. Moreover, both the cellular RNA exosome complex and a recombinant RNA exosome core complex impart robust AID- and transcription-dependent DNA deamination of both strands of transcribed SHM substrates in vitro. Our findings reveal a role for noncoding RNA surveillance machinery in generating antibody diversity.
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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.