ArticleNucleic acids research2019
Histone deacetylase 3 controls a transcriptional network required for B cell maturation.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Acetylation profiling by Iseq-Kac reveals insights into HSC aging and lineage decision.Nature chemical biology · 2025Article
- Deep Proteomics Analysis Unravels the Molecular Signatures of Tonsillar B Cells in PFAPA and OSAS in the Pediatric Population.International journal of molecular sciences · 2025Article
- Enzyme-independent functions of HDAC3 in the adult heart.Acta pharmaceutica Sinica. B · 2025Article
- Review
- Repurposing Histone Deacetylase Inhibitors for Management of Solid Organ Transplant Rejection.Results and problems in cell differentiation · 2025Review
- Mutant FOXO1 controls an oncogenic network via enhancer accessibility.Cell genomics · 2024Article
- Article
- Review
- Epigenetic regulation of B cells and its role in autoimmune pathogenesis.Cellular & molecular immunology · 2022Review
- Chidamide Suppresses the Growth of Cholangiocarcinoma by Inhibiting HDAC3 and Promoting FOXO1 Acetylation.Stem cells international · 2022Article
- Comprehensive Analysis of the Differential Expression and Prognostic Value of Histone Deacetylases in Glioma.Frontiers in cell and developmental biology · 2022Article
- Intravitreal HDAC Inhibitor Belinostat Effectively Eradicates Vitreous Seeds Without Retinal Toxicity In Vivo in a Rabbit Retinoblastoma Model.Investigative ophthalmology & visual science · 2021Article
- Inhibited HDAC3 or Elevated MicroRNA-494-3p Plays a Protective Role in Myocardial Ischemia-Reperfusion Injury via Suppression of BRD4.Molecular neurobiology · 2021Article
- Article
- Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Histone deacetylase 3 (Hdac3) is a target of the FDA approved HDAC inhibitors, which are used for the treatment of lymphoid malignancies. Here, we used Cd19-Cre to conditionally delete Hdac3 to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3-/- mice showed impaired germinal center formation along with a defect in plasmablast production. Analysis of Hdac3-/- germinal centers revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation between genes up-regulated upon Hdac3 loss and those up-regulated in Foxo1-deleted germinal center B cells, even though Foxo1 typically activates transcription. Therefore, to determine whether gene expression changes observed in Hdac3-/- germinal centers were a result of direct effects of Hdac3 deacetylase activity, we used an HDAC3 selective inhibitor and examined nascent transcription in germinal center-derived cell lines. Transcriptional changes upon HDAC3 inhibition were enriched for light zone gene signatures as observed in germinal centers. Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 function including CD86, CD83 and CXCR5 that are likely responsible for driving the light zone phenotype observed in vivo.
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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 Socratic graph.