ReviewFrontiers in molecular biosciences2023
Insights into the function of HDAC3 and NCoR1/NCoR2 co-repressor complex in metabolic diseases.
Review in Frontiers in molecular biosciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.Nature aging · 2026Article
- NCOR1 and NCOR2 Exhibit Distinct Cellular and Transcriptomic Signatures in Human Abdominal Aortic Aneurysm.Biomedicines · 2026Article
- Serpina3c protects against metabolic dysfunction-associated steatotic liver disease in offspring induced by prenatal prednisone exposure.Signal transduction and targeted therapy · 2026Article
- Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer.Journal of the National Cancer Center · 2026Review
- Metabo-epigenetic circuits of heart failure: chromatin-modifying enzymes as determinants of metabolic plasticity.EMBO molecular medicine · 2026Review
- Review
- Bifidobacterium infantis-mediated HSV-TK/GCV therapy modulates the tumor microenvironment through site-specific phosphorylation of HIF-1α, mTOR, and PD-L1.Frontiers in oncology · 2026Article
- Bioinformatics analysis identifies key secretory protein-encoding differentially expressed genes in adipose tissue of metabolic syndrome.Adipocyte · 2025Article
- From omics to AI-mapping the pathogenic pathways in type 2 diabetes.FEBS letters · 2025Review
- Deep Sequencing Reveals Novel Mutations inInternational journal of molecular sciences · 2025Article
- Epigenetic isoforms (DNMT3A/3B and HDAC3/7) potential predictors of endothelial dysfunction and subclinical atherosclerosis.Molecular biology reports · 2025Review
- Alteration in epigenetic profile in subclinical atherosclerosis and in high uric acid.Scientific reports · 2025Article
- Harnessing Nanopore Sequencing to Investigate the Epigenomic Landscape in Molar Incisor Hypomineralization-A Pilot Study.International journal of molecular sciences · 2025Article
- Androgens as the "old age stick" in skeletal muscle.Cell communication and signaling : CCS · 2025Review
- Review
- Exploring fatty acids from royal jelly as a source of histone deacetylase inhibitors: from the hive to applications in human well-being and health.Epigenetics · 2024Article
- 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
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
- The transcription factor PPARA mediates SIRT1 regulation of NCOR1 to protect damaged heart cells.Cardiovascular diagnosis and therapy · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase 3 (HDAC3) and nuclear receptor co-repressor (NCoR1/2) are epigenetic regulators that play a key role in gene expression and metabolism. HDAC3 is a class I histone deacetylase that functions as a transcriptional co-repressor, modulating gene expression by removing acetyl groups from histones and non-histone proteins. NCoR1, on the other hand, is a transcriptional co-repressor that interacts with nuclear hormone receptors, including peroxisome proliferator-activated receptor gamma (PPARγ) and liver X receptor (LXR), to regulate metabolic gene expression. Recent research has revealed a functional link between HDAC3 and NCoR1 in the regulation of metabolic gene expression. Genetic deletion of HDAC3 in mouse models has been shown to improve glucose intolerance and insulin sensitivity in the liver, skeletal muscle, and adipose tissue. Similarly, genetic deletion of NCoR1 has improved insulin resistance and reduced adiposity in mouse models. Dysregulation of this interaction has been associated with the development of cardio-metabolic diseases such as cardiovascular diseases, obesity and type 2 diabetes, suggesting that targeting this pathway may hold promise for the development of novel therapeutic interventions. In this review, we summarize the current understanding of individual functions of HDAC3 and NCoR1/2 and the co-repressor complex formation (HDAC3/NCoR1/2) in different metabolic tissues. Further studies are needed to thoroughly understand the mechanisms through which HDAC3, and NCoR1/2 govern metabolic processes and the implications for treating metabolic diseases.
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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 Socratic graph.