Response to estradiol-ERalpha ERE Binding defective mutant. Homo sapiens

In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha mutant (ERalpha 203/204/211E) that functions exclusively at the ERE-independent pathway demonstrated that genomic responses assessed by microarrays from the ERE-independent pathway to E2-ERalpha are not sufficient to alter cellular growth, death or motility. These findings suggest that the ERE-dependent pathway is the canonical E2-ERalpha signaling in model cell lines. Keywords: MDA-MB-231 cells Overall design: Cells were infected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha 203/204/211E (3411E) for 48h. Infected cells were then treated with 1 nM Estradiol 17beta for 6h. All experiments were repeated six independent times conducted at at six different days