ArticleCell death and differentiation2019
Degradation of selenoprotein S and selenoprotein K through PPARγ-mediated ubiquitination is required for adipocyte differentiation.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Yeast β-glucan selenium nanoparticles enhance meat quality in heat-stressed broilers via SelO-mediated mitochondrial biogenesis and oxidative myofiber remodeling.Journal of animal science and biotechnology · 2026Article
- Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.Journal of advanced research · 2025Article
- Selenoprotein K at the intersection of cellular pathways.Archives of biochemistry and biophysics · 2025Review
- Selenium participates in the formation of kidney stones by alleviating endoplasmic reticulum stress and apoptosis of renal tubular epithelial cells.Redox report : communications in free radical research · 2024Article
- Selenium-SelK-GPX4 axis protects nucleus pulposus cells against mechanical overloading-induced ferroptosis and attenuates senescence of intervertebral disc.Cellular and molecular life sciences : CMLS · 2024Article
- Current views on selenoprotein S in the pathophysiological processes of diabetes-induced atherosclerosis: potential therapeutics and underlying biomarkers.Diabetology & metabolic syndrome · 2024Review
- The Regulation of Selenoproteins in Diabetes: A New Way to Treat Diabetes.Current pharmaceutical design · 2024Review
- Tissue-specific mechanisms of fat metabolism that focus on insulin actions.Journal of advanced research · 2023Review
- Selenoprotein S Interacts with the Replication and Transcription Complex of SARS-CoV-2 by Binding nsp7.Journal of molecular biology · 2023Article
- Reduction of NADPH oxidase 4 in adipocytes contributes to the anti-obesity effect of dihydroartemisinin.Heliyon · 2023Article
- Lysine 222 in PPAR γ1 functions as the key site of MuRF2-mediated ubiquitination modification.Scientific reports · 2023Article
- The Potential Roles of Post-Translational Modifications of PPARγ in Treating Diabetes.Biomolecules · 2022Review
- Selenoprotein S: A versatile disordered protein.Archives of biochemistry and biophysics · 2022Review
- Review
- Selenoprotein K Is Essential for the Migration and Phagocytosis of Immature Dendritic Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation.Redox biology · 2022Article
- Trace Element Selenium Effectively Alleviates Intestinal Diseases.International journal of molecular sciences · 2021Review
- Regulation of Ferroptosis Pathway by Ubiquitination.Frontiers in cell and developmental biology · 2021Review
- Integrated Analysis to Study the Relationship between Tumor-Associated Selenoproteins: Focus on Prostate Cancer.International journal of molecular sciences · 2020Article
- The USP10-HDAC6 axis confers cisplatin resistance in non-small cell lung cancer lacking wild-type p53.Cell death & disease · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipocyte differentiation is known to be related with endoplasmic reticulum (ER) stress. We have reported that selenoprotein S (SelS) and selenoprotein K (SelK) have a function in the regulation of ER stress and ER-associated degradation. However, the association between adipocyte differentiation and the ER-resident selenoproteins, SelS and SelK, is unclear. In this study, we found that the levels of SelS and SelK were decreased during adipocyte differentiation and were inversely related to the levels of peroxisome proliferator-activated receptor γ (PPARγ), a central regulator of adipogenesis. It has been recently reported that PPARγ has E3 ubiquitin ligase activity. Here, we report that PPARγ directly interacts with both SelS and SelK via its ligand-binding domain to induce ubiquitination and degradation of the selenoproteins. Lysine residues at the 150th position of SelS and the 47th and 48th positions of SelK were the target sites for ubiquitination by PPARγ. We also found that adipocyte differentiation was inhibited when either SelS or SelK was not degraded by PPARγ. Thus, these data indicate that PPARγ-mediated ubiquitination and degradation of SelS and SelK is required for adipocyte differentiation.
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