ArticleCell reports2022
HNF4A modulates glucocorticoid action in the liver.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Cortisol drives pregnancy-associated induction of hepatic organic anion transporter 2, sodium/taurocholate cotransporting polypeptide, and organic cation transporter 1 in HepaRG cells through glucocorticoid receptor-, hepatocyte nuclear factor 1 alpha-, and hepatocyte nuclear factor 4 alpha-dependent signaling.Drug metabolism and disposition: the biological fate of chemicals · 2026Article
- Endocrine regulation of the hepatic fasting response: cues, cooperation and consequences.Nature reviews. Endocrinology · 2026Review
- The role of HNF4α in adenocarcinoma.Biochemical Society transactions · 2026Review
- Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity.Science advances · 2026Article
- Clocks on steroids: how glucocorticoid receptors tell cells the time.The Journal of endocrinology · 2026Review
- Multi-omics profiling reveals divergent biology and liver microenvironment in HCC of metastatic and de novo origin.Molecular cancer · 2026Article
- Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.Endocrine reviews · 2026Review
- Genetic variation shapes the chromatin accessibility landscape and transcriptional responses in mouse adipose tissue.PLoS genetics · 2026Article
- Glucocorticoid-dependence and independence of the circadian liver transcriptome.Npj biological timing and sleep · 2026Article
- Review
- Quinoa Improves Non-Alcoholic Fatty Liver Disease by Regulating the Ras-PLD Pathway to Activate Autophagy.Food science & nutrition · 2025Article
- Coregulators determine androgen receptor activity in prostate cancer.Bioscience reports · 2025Review
- Hepatocyte nuclear factor 4-Alpha: a key regulator in liver carcinogenesis.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Sex-Specific Concordance of Striatal Transcriptional Signatures of Opioid Addiction in Human and Rodent Brains.Biological psychiatry global open science · 2025Article
- HNF4A mitigates sepsis-associated lung injury by upregulating NCOR2/GR/STAB1 axis and promoting macrophage polarization towards M2 phenotype.Cell death & disease · 2025Article
- HNF4α contributes to hepatic CAR dysfunction in polymicrobial sepsis.Frontiers in immunology · 2025Article
- Uncovering Potential Biomarkers and Constructing a Prediction Model Associated with Iron Metabolism in Parkinson's Disease.Neuropsychiatric disease and treatment · 2025Article
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- A critical role for HNF4α in polymicrobial sepsis-associated metabolic reprogramming and death.EMBO molecular medicine · 2024Article
- Unlocking therapeutic potential: exploring cross-talk among emerging nuclear receptors to combat metabolic dysfunction in steatotic liver disease.npj metabolic health and disease · 2024Review
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Authors and funding
8 authors.
Funding
Abstract
The glucocorticoid receptor (GR) is a nuclear receptor critical to the regulation of energy metabolism and inflammation. The actions of GR are dependent on cell type and context. Here, we demonstrate the role of liver lineage-determining factor hepatocyte nuclear factor 4A (HNF4A) in defining liver specificity of GR action. In mouse liver, the HNF4A motif lies adjacent to the glucocorticoid response element (GRE) at GR binding sites within regions of open chromatin. In the absence of HNF4A, the liver GR cistrome is remodeled, with loss and gain of GR recruitment evident. Loss of chromatin accessibility at HNF4A-marked sites associates with loss of GR binding at weak GRE motifs. GR binding and chromatin accessibility are gained at sites characterized by strong GRE motifs, which show GR recruitment in non-liver tissues. The functional importance of these HNF4A-regulated GR sites is indicated by an altered transcriptional response to glucocorticoid treatment in the Hnf4a-null liver.
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