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. Author manuscript; available in PMC: 2009 Aug 13.
Published in final edited form as: Mol Cell Endocrinol. 2008 Apr 20;290(1-2):24–30. doi: 10.1016/j.mce.2008.04.003

Figure 2. The non-classical ERα knock-in mutation.

Figure 2

(A) Schematic illustration of the introduced double mutation (E at position 207 to A and G at position 208 to A) in the first zinc finger of the DNA-binding domain of mouse ERα. (B,C) Transfection studies were performed in ER-deficient TSA cells, using either ERE (B) or AP1 (C) reporters. Cells were transfected with WT ERα or the E207A/G208A mutant. Cells were treated with ethanol vehicle, 1 nM E2, or 100 nM ICI 182,780, and luciferase activity was measured. The E207A/G208A mutant was incapable of activating transcription through EREs but retained the full capacity to activate transcription through AP1. (Jakacka et al., 2002)