ArticleInternational journal of molecular sciences2014
KCNK10, a tandem pore domain potassium channel, is a regulator of mitotic clonal expansion during the early stage of adipocyte differentiation.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 35 citations in OpenAlex.
- C/EBPδ as a Regulatory Node in Adipocytes: Roles in Differentiation, Metabolism, and Immune Function.Biomolecules · 2026Review
- Novel function of TREK-1 in regulating adipocyte differentiation and lipid accumulation.Cell death & disease · 2025Article
- Combined effects of genetic background and diet on mouse metabolism and gene expression.iScience · 2024Article
- Down-Regulation of CYP3A4 by the KInternational journal of molecular sciences · 2023Article
- Insights into the architecture of human-induced polygenic selection in Duroc pigs.Journal of animal science and biotechnology · 2022Article
- Bioelectrical controls of morphogenesis: from ancient mechanisms of cell coordination to biomedical opportunities.Current opinion in genetics & development · 2019Review
- KCa1.1 channels regulate βFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
KCNK10, a member of tandem pore domain potassium channel family, gives rise to leak K+ currents. It plays important roles in stabilizing the negative resting membrane potential and in counterbalancing depolarization. We previously demonstrated that kcnk10 expression is quickly elevated during the early stage of adipogenesis of 3T3-L1 cells and that reduction of kcnk10 expression inhibits adipocyte differentiation. However, the molecular mechanism of KCNK10 in adipocyte differentiation remains unclear. Here we revealed that kcnk10 is induced by 3-isobutyl-1-methylxanthine, a cyclic nucleotide phosphodiesterase inhibitor and a potent inducer of adipogenesis, during the early stage of adipocyte differentiation. We also demonstrated that KCNK10 functions as a positive regulator of mitotic clonal expansion (MCE), a necessary process for terminal differentiation. The reduction of kcnk10 expression repressed the expression levels of CCAAT/enhancer-binding protein β (C/EBPβ) and C/EBPδ as well as the phosphorylation level of Akt during the early phase of adipogenesis. In addition, knockdown of kcnk10 expression suppressed insulin-induced Akt phosphorylation. These results indicate that KCNK10 contributes to the regulation of MCE through the control of C/EBPβ and C/EBPδ expression and insulin signaling.
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