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. 2020 Jan 16;11(1):31. doi: 10.1038/s41419-020-2225-6

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© The Author(s) 2020

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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Fig. 5 — a Nuclear and cytosolic fractionation analysis for endogenous TKT in SMMC-7721 cells with aberrant expression of STAT1. b Nuclear and cytosolic fractionation analysis for endogenous TKT in SMMC-7721 cells with STAT1 shRNA. c Immunofluorescent localization of TKT in SMMC-7721 cells with knockdown STAT1. d Luciferase activity analysis of the 2.5 kb FXR promoter at 48 h after the FXR promoter plasmid and empty vector or TKT-shRNA expression plasmids were transfected into the stable overexpression STAT1 cell line SMMC-7721. e Luciferase activity analysis of the 2.5 kb FXR promoter at 48 h after the FXR promoter plasmid and empty vector or STAT1-shRNA expression plasmids were transfected into SMMC-7721. Data are presented as mean ± squared error (SEM), the bar indicates the mean. Statistical significance was calculated using two-tailed unpaired t-test, *p < 0.05, **p < 0.01, ***p < 0.001. f Western blot analysis of FXR, STAT1, and TKT expression after STAT1-shRNA expression plasmids were transfected into SMMC-7721.