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. 2015 Jan 16;123(5):493–499. doi: 10.1289/ehp.1408586

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Luciferase activity in cells transfected with a luciferase reporter plasmid and treated with vehicle (–), 100 nmol/L E2, 1 μmol/L atrazine (Atr), 10 μmol/L ICI (ER antagonist), E2 + ICI, or Atr + ICI. ERα transactivation in BG-1 (A), MCF-7 (B), or Ishikawa (C) cells transfected with ERE-luc before treatment. (D–F) SkBr3 cells transfected with ERE-luc and ERα expression plasmid (D), Gal4 reporter gene (GK1) plus the Gal4 fusion proteins encoding the hormone-binding domain of ERα (GalERα; E), or GK1 plus GalERβ (F) before treatment. Luciferase activity was normalized to the internal transfection control, and values for vehicle controls were set as 1-fold induction. Values shown are mean ± SD of three independent experiments performed in triplicate. *p < 0.05 compared with vehicle treatment.