ArticleJournal of cellular and molecular medicine2018
NR4A1 retards adipocyte differentiation or maturation via enhancing GATA2 and p53 expression.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Multi-omic responses to acute exercise in abdominal subcutaneous adipose tissue of sedentary adults: findings from MoTrPAC.bioRxiv : the preprint server for biology · 2026Article
- METTL14 and WTAP play a crucial role in the regulation of bovine preadipocyte differentiation.Animal biotechnology · 2025Article
- RNA Sequencing and Metabolomic Analyses Reveal Differences in Muscle Characteristics and Metabolic Profiles Between Purebred and Crossbred Huainan Pigs.Animals : an open access journal from MDPI · 2025Article
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Orphan nuclear receptor NR4A1 regulates both osteoblastogenesis and adipogenesis in human mesenchymal stem cells.Molecular medicine reports · 2025Article
- Transcriptional Dynamics and Key Regulators of Adipogenesis in Mouse Embryonic Stem Cells: Insights from Robust Rank Aggregation Analysis.International journal of molecular sciences · 2024Article
- Identification of key genes affecting intramuscular fat deposition in pigs using machine learning models.Frontiers in genetics · 2024Article
- High-Fat Diet Promotes Adipogenesis in Offspring Female Rats Induced by Perinatal Exposure to 4-Nonylphenol.BioMed research international · 2023Article
- Mesenchymal stem cells-derived extracellular vesicles containing miR-378a-3p inhibit the occurrence of inflammatory bowel disease by targeting GATA2.Journal of cellular and molecular medicine · 2022Article
- Knockout of Nur77 Leads to Amino Acid, Lipid, and Glucose Metabolism Disorders in Zebrafish.Frontiers in endocrinology · 2022Article
- Adipose-derived mesenchymal stem cells differentiate into pancreatic cancer-associated fibroblasts in vitro.FEBS open bio · 2020Article
- Targeting Orphan Nuclear Receptors NR4As for Energy Homeostasis and Diabetes.Frontiers in pharmacology · 2020Review
- Function of Nr4a Orphan Nuclear Receptors in Proliferation, Apoptosis and Fuel Utilization Across Tissues.Cells · 2019Review
- NR4A1 retards adipocyte differentiation or maturation via enhancing GATA2 and p53 expression.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear receptor subfamily 4 group A member 1 (NR4A1) is an orphan nuclear receptor with diverse functions. It has been reported that NR4A1, as a transcriptional activator, is implicated in glucose and lipid metabolism. The aim of this study was to investigate the regulatory role of NR4A1 in adipogenesis and explore the underlying mechanisms. Quantitative real-time PCR and Western blotting were used to analyse the expression of genes involved in synthesis and mobilization of fats in vivo and in vitro. Dual-luciferase reporter assay was conducted to study the regulatory mechanisms of NR4A1. Our data from in vivo study confirmed that NR4A1 knockout (KO) mice fed with high-fat diet were more prone to obesity, and gene expression levels of PPARγ and FAS were increased in KO mice compared to controls; our data from in vitro study showed that NR4A1 overexpression in 3T3-L1 pre-adipocytes inhibited adipogenesis. Moreover, NR4A1 enhanced GATA binding protein 2 (GATA2) expression, which in turn inhibited peroxisome proliferator-activated receptor γ (PPARγ); NR4A1 inhibited sterol regulatory element binding transcription factor 1 (SREBP1) and its downstream gene fatty acid synthase (FAS) by up-regulating p53. NR4A1 inhibits the differentiation and lipid accumulation of adipocytes by enhancing the expression of GATA2 and p53.
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