ArticleNature communications2017
An HDAC3-PROX1 corepressor module acts on HNF4α to control hepatic triglycerides.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 68 citations in OpenAlex.
- BHLHE40 and ChREBP associate with hepatic enhancer clusters containing PPARα, RXRα, and HNF4 nuclear receptors.Endocrinology · 2026Article
- CLOCK/BMAL1 interactome uncovers homeodomain factors as tissue regulators.Nature cell biology · 2026Article
- Ligand-dependent reprogramming of HNF4A expression and function suppresses multistep hepatocarcinogenesis.Molecular therapy. Oncology · 2026Article
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
- Sex-specific KDM6A-HNF4A-CREBH network controls lipoprotein cholesterol metabolism and atherosclerosis via epigenetic reprograming of hepatocytes.Nature communications · 2026Article
- Endothelial PROX1 induces blood-brain barrier disruption in the central nervous system.JCI insight · 2026Article
- Chidamide enhances the sensitivity of gastric cancer to 5-fluorouracil chemotherapy by suppressing the HDAC3/HNF4A/TYMS axis.Cell death & disease · 2025Article
- Downregulation of the NF-κB protein p65 is a shared phenotype among most anti-aging interventions.GeroScience · 2025Article
- Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis.Nature genetics · 2025Article
- Inhibition of triglyceride metabolism-associated enhancers alters lipid deposition during adipocyte differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- ERRα and ERRγ coordinate expression of genes associated with Alzheimer's disease, inhibitingProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Downregulation of HNF4A enables transcriptomic reprogramming during the hepatic acute-phase response.Communications biology · 2024Article
- Nuclear receptor corepressors non-canonically drive glucocorticoid receptor-dependent activation of hepatic gluconeogenesis.Nature metabolism · 2024Article
- HDAC3 and HDAC8 PROTAC dual degrader reveals roles of histone acetylation in gene regulation.Cell chemical biology · 2023Article
- Article
- Coordinated transcriptional upregulation of oxidative metabolism proteins in long-lived endocrine mutant mice.GeroScience · 2023Article
- Single-cell analysis of lymphatic endothelial cell fate specification and differentiation during zebrafish development.The EMBO journal · 2023Article
- Caloric restriction remodels the hepatic chromatin landscape and bile acid metabolism by modulating the gut microbiota.Genome biology · 2023Article
- The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases.Cell death discovery · 2023Review
- Hepatic metabolism of grazing cows of two Holstein strains under two feeding strategies with different levels of pasture inclusion.PloS one · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The histone deacetylase HDAC3 is a critical mediator of hepatic lipid metabolism, and liver-specific deletion of HDAC3 leads to fatty liver. To elucidate the underlying mechanism, here we report a method of cross-linking followed by mass spectrometry to define a high-confidence HDAC3 interactome in vivo that includes the canonical NCoR-HDAC3 complex as well as Prospero-related homeobox 1 protein (PROX1). HDAC3 and PROX1 co-localize extensively on the mouse liver genome, and are co-recruited by hepatocyte nuclear factor 4α (HNF4α). The HDAC3-PROX1 module controls the expression of a gene program regulating lipid homeostasis, and hepatic-specific ablation of either component increases triglyceride content in liver. These findings underscore the importance of specific combinations of transcription factors and coregulators in the fine tuning of organismal metabolism.HDAC3 is a critical mediator of hepatic lipid metabolism and its loss leads to fatty liver. Here, the authors characterize the liver HDAC3 interactome in vivo, provide evidence that HDAC3 interacts with PROX1, and show that HDAC3 and PROX1 control expression of genes regulating lipid homeostasis.
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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.