ArticleMolecular cell2013
Deacetylase-independent function of HDAC3 in transcription and metabolism requires nuclear receptor corepressor.
Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.
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Who cites it
165 citing papers in PubMed, 252 citations in OpenAlex.
- Targeting epigenetic regulators induces transcription-replication conflicts to overcome ATR inhibitor resistance.Nucleic acids research · 2026Article
- HDAC3 as an Immunometabolic Rheostat: Molecular Mechanisms of Deacylation Plasticity, Lactylation Dynamics, and Spatiotemporal Regulation.Biomolecules · 2026Review
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
- Endometrial NCOR1 deficiency contributes to implantation failure in endometriosis-associated infertility.iScience · 2026Article
- NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer.Nature communications · 2026Article
- Nuclear receptor coregulator interactions: beyond the switch.Genes & development · 2026Review
- CRISPR Screen Identifies HDAC3 as a Novel Radiosensitizing Target in Small Cell Lung Cancer.Molecular cancer therapeutics · 2026Article
- Catalytic-independent roles of chromatin modifiers in mammalian development and the implications for treating human disease.Biochemical Society transactions · 2025Review
- Article
- Epigenetic dysregulation of energy homeostasis drives aortic valve stenosis that is treatable with metformin.JCI insight · 2025Article
- SMRT anchors the HDAC3 corepressor complex to chromatin to regulate inflammatory and metabolic pathways in macrophages.Nucleic acids research · 2025Article
- Enzyme-independent functions of HDAC3 in the adult heart.Acta pharmaceutica Sinica. B · 2025Article
- Downregulation of the NF-κB protein p65 is a shared phenotype among most anti-aging interventions.GeroScience · 2025Article
- Nonproteolytic ubiquitination regulates chromatin occupancy by the NCoR/SMRT/HDAC3 corepressor complex in MCF-7 breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic Mechanisms in the Transcriptional Regulation of Circadian Rhythm in Mammals.Biology · 2025Review
- Transcriptional Cofactors for Thyroid Hormone Receptors.Endocrinology · 2025Review
- HDAC3 in action: Expanding roles in inflammation and inflammatory diseases.Cell proliferation · 2025Review
- Nuclear receptor corepressor 1 levels differentially impact the intracellular dynamics of mutant thyroid hormone receptors associated with resistance to thyroid hormone syndrome.Molecular and cellular endocrinology · 2024Article
- Transcriptional repression by HDAC3 mediates T cell exclusion fromProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
105 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) are believed to regulate gene transcription by catalyzing deacetylation reactions. HDAC3 depletion in mouse liver upregulates lipogenic genes and results in severe hepatosteatosis. Here we show that pharmacologic HDAC inhibition in primary hepatocytes causes histone hyperacetylation but does not upregulate expression of HDAC3 target genes. Meanwhile, deacetylase-dead HDAC3 mutants can rescue hepatosteatosis and repress lipogenic genes expression in HDAC3-depleted mouse liver, demonstrating that histone acetylation is insufficient to activate gene transcription. Mutations abolishing interactions with the nuclear receptor corepressor (NCOR or SMRT) render HDAC3 nonfunctional in vivo. Additionally, liver-specific knockout of NCOR, but not SMRT, causes metabolic and transcriptomal alterations resembling those of mice without hepatic HDAC3, demonstrating that interaction with NCOR is essential for deacetylase-independent function of HDAC3. These findings highlight nonenzymatic roles of a major HDAC in transcriptional regulation in vivo and warrant reconsideration of the mechanism of action of HDAC inhibitors.
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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.