ArticleGenes & development2014
Thrap3 docks on phosphoserine 273 of PPARγ and controls diabetic gene programming.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
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- Gene expression profiling and protein-protein network analysis revealed prognostic hub biomarkers linking cancer risk in type 2 diabetic patients.Scientific reports · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Thrap3 promotes nonalcoholic fatty liver disease by suppressing AMPK-mediated autophagy.Experimental & molecular medicine · 2023Article
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- Identification of Type 2 Diabetes Biomarkers From Mixed Single-Cell Sequencing Data With Feature Selection Methods.Frontiers in bioengineering and biotechnology · 2022Article
- Three decades of Cdk5.Journal of biomedical science · 2021Review
- Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis.BMC cardiovascular disorders · 2021Article
- PPARγ and Diabetes: Beyond the Genome and Towards Personalized Medicine.Current diabetes reports · 2021Review
- The Pluripotent Activities of Caffeic Acid Phenethyl Ester.Molecules (Basel, Switzerland) · 2021Review
- Inhibition of a Novel CLK1-THRAP3-PPARγ Axis Improves Insulin Sensitivity.Frontiers in physiology · 2021Article
- Peroxisome proliferator-activated receptor agonists and reversal of vascular degeneration through DNA repair, a step toward drug-induced regenerative medicine.Cardiovascular endocrinology & metabolism · 2020Review
- Triphenyl phosphate is a selective PPARγ modulator that does not induce brite adipogenesis in vitro and in vivo.Archives of toxicology · 2020Article
- A role for alternative splicing in circadian control of exocytosis and glucose homeostasis.Genes & development · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Phosphorylation of peroxisome proliferator-activated receptor γ (PPARγ) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance, but the underlying molecular mechanisms are unclear. We show here that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPARγ when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programming mediated by the phosphorylation of PPARγ. Knockdown of Thrap3 restores most of the genes dysregulated by CDK5 action on PPARγ in cultured adipocytes. Importantly, reduced expression of Thrap3 in fat tissue by antisense oligonucleotides (ASOs) regulates a specific set of genes, including the key adipokines adiponectin and adipsin, and effectively improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight. These data indicate that Thrap3 plays a crucial role in controlling diabetic gene programming and may provide opportunities for the development of new therapeutics for obesity and type 2 diabetes.
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Registered trials
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.