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. Author manuscript; available in PMC: 2019 Jul 15.
Published in final edited form as: Mol Cell Endocrinol. 2017 Oct 9;470:127–141. doi: 10.1016/j.mce.2017.10.005

Fig. 11. AKR1D1 promoter was transrepressed by PPARα activation.

Fig. 11

(A) AKR1D1 promoter reporter, phAKR1D1(-5kb), was co-transfected into HepG2 cells with nuclear receptor FXRα1, (B) FXRα2, (C) LXRα, (D) PPARα, (E) PPARβ or (F) PPARγ, followed by treatment with corresponding nuclear receptor agonists GW4064 (1μM) for FXRα1 and FXRα2, GW3965 (1μM) for LXRα, GW7647 (10μM) for PPARα, GW0742 for PPARβ and pioglitazone (PGZN) for PPARγ for 30h. AKR1D1 promoter transactivation levels were quantified by the dual luciferase assays. The experiments were independently repeated at least once with each experiment having triplicates for each treatment. * p<0.05 with Student’s t-test.