Fig 1.

 HREs in intron E of FKBP5 confer glucocorticoid and progestin, but not androgen, responsiveness. (A) T-47D cells were transfected with a luciferase-reporter plasmid driven by the FKBP5 promoter (p3540) or 1 of 2 fragments of intron E of FKBP5 fused upstream of the SV40 promoter in pGL3-Promoter (pIE1 and pIE2) and treated with vehicle or 10-nM R5020. (B) A549 cells were transfected with the luciferase-reporter plasmids p3540, pIE1, pIE2, or a luciferase-reporter plasmid driven by the human αENaC promoter (ENaC), and treated with vehicle or 10-nM dexamethasone. (C) LNCaP cells were transfected with luciferase-reporter plasmids p3540Luc, pIE1, pIE2, or a luciferase-reporter plasmid driven by the human prostate-specific antigen enhancer, and treated with vehicle or 10-nM dihydrotestosterone. After 24 hours, cells were collected for assay of luciferase activity, and the data are expressed as fold induction over untreated cells. Each bar represents the mean ± SEM of 3 independent experiments. HRE, hormone response element; PSE, prostate-specific antigen enhancer