Figure 1.

The −125 to −82 region of the TNF-α promoter is required for E₂ repression. A deletion series of the human TNF-α promoter (3 μg) was transiently transfected individually into U937 cells with 1 μg of expression vector for human ERα (A) or ERβ485 (B). Cells were treated for 24 h with TNF-α (5 ng/ml) in the absence or presence of 10 nM E₂, and luciferase activity was measured. (C) ERβ is more potent than ERα at repressing TNF-α activation of the TNF-RE. U937 cells were transfected with 3 μg of TNF-RE TKLuc and 1 μg of human ERα, ERβ485, or ERβ530. Cells were treated for 24 h with TNF-α (5 ng/ml) in the presence of increasing concentrations of E₂, and luciferase activity was measured. (D) ERα is more effective than ERβ at activating an ERE. U937 cells were transfected with 3 μg of ERE TKLuc and 1 μg of human ERα, ERβ485, or ERβ530. Cells were maintained in the absence or presence of 10 nM E₂ for 24 h and then assayed for luciferase activity.