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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Expert Opin Drug Metab Toxicol. 2019 Mar 18;15(4):329–339. doi: 10.1080/17425255.2019.1588884

Figure 2. Regulation of EST by nuclear receptors.

Figure 2.

Normally, EST has a low expression in some tissues, such as the liver. Upon the presence of a ligand (L), that can be either dexamethasone, GW3965, or TCPOPBOP, the nuclear receptors GR, LXR, or CAR, respectively, can bind to the promoter region of the EST gene and increase its expression in the liver. * indicates that the induction only occurs in livers of female mice. In contrast, retinoid X receptor alpha (RXRα) suppresses the expression of EST in the presence of its agonists Bexarotene (BEX). Similarly, upon the binding of its agonist rifampicin (RIF), pregnane X receptor (PXR) binds to the transcription factor hepatocyte nuclear factor 4α (HNF4α), which culminates with the downregulation of EST. Additionally, agonists for farnesoid X receptor (FXR), such as GW4064, prevent the binding of PGC1α to HNF4α, also leading to EST downregulation.