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. 2014 Apr;42(4):796–802. doi: 10.1124/dmd.113.055178

Fig. 3.

Fig. 3.

Putative cis-element responsible for SULT2A1 induction by E2 is located within -257/+140. (A) HepG2 cells were cotransfected with a 5′-deletion construct of pGL3-SULT2A1, ERα expression plasmid, and pCMV-Renilla. The transfected cells were treated with vehicle (ethanol) or E2 (100 nM), and luciferase assay was performed. *P < 0.05; ***P < 0.001 versus pGL3-SULT2A1. (B) Putative ERα or AP-1 binding sites within –257/+140 upstream region of SULT2A1 are shown. National Center for Biotechnology Information reference sequence NG_016745.1 was used. (C) HepG2 cells were cotransfected with pGL3-SULT2A1 (–257/+140) harboring mutations in S1, S2, and/or S3 (represented by a black box); ERα expression plasmid, and pCMV-Renilla. The transfected cells were treated with vehicle (ethanol) or E2 (100 nM), and luciferase assay was performed. ***P < 0.001 versus wild-type pGL3-SULT2A1 (–257/+140). (D) HepG2-ER cells were treated with E2 (100 nM) for 45 minutes, and cell lysates were collected. ChIP assays were carried out using rabbit IgG or an antibody against ERα, and the amount of ERα-bound DNA was measured by qRT-PCR using primer sets that amplify –128/–23 of SULT2A1 or –487/–381 of TFF1. **P < 0.01.