ArticleProceedings of the National Academy of Sciences of the United States of America2011
Histone chaperone Spt6 is required for class switch recombination but not somatic hypermutation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. 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, 44 citations in OpenAlex.
- 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
- Insights on SNPs of Human Activation-Induced Cytidine Deaminase AID.International journal of molecular sciences · 2025Review
- The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024Review
- Insights into Spt6: a histone chaperone that functions in transcription, DNA replication, and genome stability.Trends in genetics : TIG · 2023Review
- The conserved histone chaperone Spt6 is strongly required for DNA replication and genome stability.Cell reports · 2023Article
- AFF3, a susceptibility factor for autoimmune diseases, is a molecular facilitator of immunoglobulin class switch recombination.Science advances · 2022Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- Transient AID expression for in situ mutagenesis with improved cellular fitness.Scientific reports · 2018Article
- Histone methyltransferase MMSET promotes AID-mediated DNA breaks at the donor switch region during class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.Scientific reports · 2017Article
- A Novel Regulator of Activation-Induced Cytidine Deaminase/APOBECs in Immunity and Cancer: Schrödinger's CATalytic Pocket.Frontiers in immunology · 2017Review
- Functional requirements of AID's higher order structures and their interaction with RNA-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Chromatin remodeller SMARCA4 recruits topoisomerase 1 and suppresses transcription-associated genomic instability.Nature communications · 2016Article
- Article
- Accumulation of the FACT complex, as well as histone H3.3, serves as a target marker for somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Regulation of Aicda expression and AID activity.Autoimmunity · 2013Review
- Spt6 prevents transcription-coupled loss of posttranslationally modified histone H3.Scientific reports · 2013Article
- GANP regulates recruitment of AID to immunoglobulin variable regions by modulating transcription and nucleosome occupancy.Nature communications · 2013Article
- Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.Immune network · 2012Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID) is shown to be essential and sufficient to induce two genetic alterations in the Ig loci: class switch recombination (CSR) and somatic hypermutation (SHM). However, it is still unknown how a single-molecule AID differentially regulates CSR and SHM. Here we identified Spt6 as an AID-interacting protein by yeast two-hybrid screening and immunoprecipitation followed by mass spectrometry. Knockdown of Spt6 resulted in severe reduction of CSR in both the endogenous Ig locus in B cells and an artificial substrate in fibroblast cells. Conversely, knockdown of Spt6 did not reduce but slightly enhanced SHM in an artificial substrate in B cells, indicating that Spt6 is required for AID to induce CSR but not SHM. These results suggest that Spt6 is involved in differential regulation of CSR and SHM by AID.
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