Forskolin Stimulates Estrogen Receptor (ER) α Transcriptional Activity and Protects ER from Degradation by Distinct Mechanisms

Figure 2

Forskolin increases ERα-mediated transcription via the ligand-binding domain (LBD). (a) The upper panel is a schematic representation of full-length rat ERα and deletion mutants used in this study. Key functional domains, including the activation function-1(AF-1), the DNA-binding domain (DBD), and the LBD/activation function-2 (AF-2) are indicated on the top. (b) HT22 cells were similarly transfected with pGL3-2ERE luciferase reporter (500 ng) plus an expressing vector carrying wild-type or mutated ERα with deletion of A/B (ΔA/B), E/F (ΔE/F), helix12/F (ΔH12/F), and F (ΔF) (10 ng) and treated either vehicle (V), estradiol (E, 10 nM), or forskolin (F, 1 μM) for 24 h. The luciferase activity (mean ± SEM) was normalized and expressed as fold stimulation over vehicle-treated groups carrying the same ER constructs (as 1 fold). , vs. vehicle-treated groups with the same expression vector.

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