The Function of the c-Myb-, Ets-, and GR-Binding Sites in the Hormone Responsiveness of the −4559/−4525 hGR Region
A, A PU.1 expression plasmid was cotransfected into Jurkat cells with the long upstream sequence (−4898/−3609) and the GRU (−4559/−4525) linked to a luciferase reporter gene, together with the GR expression plasmid and the β-gal construct, as described in the legend of Fig. 2. The hormone-stimulated promoter expression is presented as percent of its respective EtOH vehicle control. ***, P < 0.005. B, Overexpression of a dominant-negative DNA binding inhibitor of c-Ets or c-Myb blunts the hormonal response of the GRU. ***, P < 0.005 compared with the EtOH control. C, Basal promoter activity [in relative light units (RLU)] and hormonal responsiveness of the minimal GRU with the deletion of the c-Myb or EBE1/GR recognition sequences (Jurkat cells). Hormone responsiveness is plotted as percent of EtOH-treated controls for each reporter construct, respectively. ***, P < 0.005.