Estrogen Receptor β Activates the Human Retinoic Acid Receptorα -1 Promoter in Response to Tamoxifen and Other Estrogen Receptor Antagonists, but Not in Response to Estrogen
1999
Human estrogen receptor-α (hERα) or -β (hERβ) transfected into Hep G2 or COS1 cells each responded to estrogen to increase transcription from an estrogen-responsive element (ERE)-driven reporter vector with similar fold induction through a classical mechanism involving direct receptor binding to DNA. ER antagonists inhibited this estrogen induction through both hERα and hERβ, although raloxifene was more potent through ERα than ERβ, and tamoxifen was more potent via ERβ than ERα. We have shown previously that estrogen stimulated the human retinoic acid receptor-α-1 (hRARα-1) promoter through nonclassical EREs by a mechanism that was ERα dependent, but that did not involve direct receptor binding to DNA. We show here that in contrast to hERα, hERβ did not induce reporter activity driven by the hRARα-1 promoter in the presence of estrogen. While hERβ did not confer estrogen responsiveness on this promoter, it did elicit transcriptional activation in the presence of 4-hydroxytamoxifen (4-OH-Tam). Additionall...
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