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. 2021 Oct 15;8:711398. doi: 10.3389/fnut.2021.711398

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Copyright © 2021 Liu, Gu, Li, Hu, Yang, Li, Li, Zhang, Zhou, Wu, Bao and Cai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PPARα mediates REV-ERBα transcriptional activation. (A–C) PPARα binding to the enhancer of Nr1d1 (upper panel) and the promoter of Nr1d1 (lower panel) determined by ChIP-qPCR in the hepatocytes of vehicle control, CLA, or cotreatment of CLA with PPARα antagonists (GW6471, MK866) in (A), or cotreatment of CLA with REV-ERBα antagonists (SR8278, GSK1362) in (B), or CLA with PPARα knockdown in (C). (D) Relative enrichment of histone marks H3K27ac and H3K4me1, and Pol-II and Ser2P Pol-II recruitment at the enhancer of Nr1d1. (E) Relative enrichment of histone marks H3K27ac and H3K4me3, and Pol-II and Ser5P Pol-II recruitment at the promoter of Nr1d1. The data are shown as the means ± SD, n = 6 per group. The experiments were repeated three times. *p < 0.05, ***p < 0.001, using ANOVA with Tukey's post-hoc test.