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. 2017 Nov 1;7:14876. doi: 10.1038/s41598-017-13974-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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TUDCA modulates IDE expression in HepG2 cells by a S1PR2 -IR receptor pathway. Protein expression of IDE in HepG2 cells treated or not with different concentrations of TUDCA for 24-h (A). Effect of TUDCA on IDE expression in the presence of 10 µM sphingosine-1-phosphate receptor 2 inhibitor (JTE-013) (B), 0.1 µM insulin receptor inhibitor (S961) (C) and 5 µM of Akt inhibitor (MK2206) or 0.1 µM of PI3k inhibitor (Wortmannin) (D). Data are mean ± SEM (n = 4–6). *P ≤ 0.05 vs control conditions.