ArticleCell2011
Class IIa histone deacetylases are hormone-activated regulators of FOXO and mammalian glucose homeostasis.
Article in Cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 342 papers, 2 of them syntheses that pooled it.
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Who cites it
342 citing papers in PubMed, 2 syntheses or guidelines pooled it, 550 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Histone deacetylase-mediated regulation of endolysosomal pH.The Journal of biological chemistry · 2018Pooled it
- Glucagon Decreases IGF-1 Bioactivity in Humans, Independently of Insulin, by Modulating Its Binding Proteins.The Journal of clinical endocrinology and metabolism · 2017Trial
- AMPK-Directed Therapeutics for MASLD: Mechanistic Rationale, Activator Classes, and Clinical Translation.International journal of molecular sciences · 2026Review
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- AMPK Therapy-A Little Goes A Long Way.Cells · 2026Review
- Iron overload suppresses LKB1 and induces IL36G anti-tumor immunity in PDAC metastasis.Science advances · 2026Article
- Comprehensive mass spectrometry screening-derived atlas of HDAC inhibitors reveals histone-specific acetylation changes.Cell reports · 2026Article
- Hepatic Gluconeogenesis and the Antidepressant Effects of Exercise: A Narrative Review.Metabolites · 2026Review
- [Research progress in mechanisms of dietary resistant starch for regulating glucose and lipid metabolism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Review
- Effects of AMPK/PGC-1α on gluconeogenesis in skeletal muscle of animals under overwintering starvation and its molecular mechanism: review.Animal bioscience · 2026Article
- HDAC5 deficiency induces intrinsic resistance to KRAS inhibition by disrupting c-Myc acetylation-ubiquitination homeostasis.The Journal of clinical investigation · 2026Article
- Myeloid HDAC7 drives liver inflammation and systemic glucose dysregulation during diet-induced obesity.Clinical & translational immunology · 2026Article
- CK2-mediated HDAC5 shuttling regulates DNA end resection through Ku70 deacetylation.Theranostics · 2026Article
- Thermal shift engagement assay for Class IIA histone deacetylase inhibitor screening.Results in chemistry · 2025Article
- Genetic adaptations shaping survival, pregnancy, and life at high altitude and sea level.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Role of adiponectin and its receptors AdipoR1/2 in inflammatory bowel disease.Cell communication and signaling : CCS · 2025Review
- HDAC4: an emerging target in diabetes mellitus and diabetic complications.European journal of medical research · 2025Review
- DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis.Nucleic acids research · 2025Article
- Association between serum beta-hydroxybutyrate levels and risk of type 2 diabetes mellitus in patients with impaired fasting glucose.Nutrition & diabetes · 2025Article
282 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
Class IIa histone deacetylases (HDACs) are signal-dependent modulators of transcription with established roles in muscle differentiation and neuronal survival. We show here that in liver, class IIa HDACs (HDAC4, 5, and 7) are phosphorylated and excluded from the nucleus by AMPK family kinases. In response to the fasting hormone glucagon, class IIa HDACs are rapidly dephosphorylated and translocated to the nucleus where they associate with the promoters of gluconeogenic enzymes such as G6Pase. In turn, HDAC4/5 recruit HDAC3, which results in the acute transcriptional induction of these genes via deacetylation and activation of FOXO family transcription factors. Loss of class IIa HDACs in murine liver results in inhibition of FOXO target genes and lowers blood glucose, resulting in increased glycogen storage. Finally, suppression of class IIa HDACs in mouse models of type 2 diabetes ameliorates hyperglycemia, suggesting that inhibitors of class I/II HDACs may be potential therapeutics for metabolic syndrome.
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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.