Figure 6.
K206 mutations abrogate the ability of ERα to titrate a repressive function from PR. (Insert) The experimental system: HeLa cells were co-transfected with a TAT3-Luc reporter that contains three progestin response elements (PREs), a PR expression vector (5 μg), and a CMV β-galactosidase internal control (2 μg). Transfections also included ERα, ERα K206 mutants or empty pSG5 vector ("No ER"; 5 μg each). (Graph) All cells were treated with the PR antagonist RU486 (10-6 M), which promotes recruitment of repressive functions to DNA by PR. The repressive functions are competed for by the ER-bound anti-estrogens, as indicated. The data is expressed as relative luciferase activity, where the ratio of luciferase activity to β-galactosidase activity in the absence of ER ligand is set to a value of 1.