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Molecular Endocrinology, doi:10.1210/me.2002-0072
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Molecular Endocrinology 16 (10): 2202-2214
Copyright © 2002 by The Endocrine Society

Signal Transducers and Activators of Transcription as Downstream Targets of Nongenomic Estrogen Receptor Actions

Linda Björnström and Maria Sjöberg

Department of Cell and Molecular Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden

Address all correspondence and requests for reprints to: Dr. Maria Sjöberg, Department of Cell and Molecular Biology, Karolinska Institute, S-171 Stockholm, Sweden. E-mail: maria.sjoberg{at}cmb.ki.se.

17ß-Estradiol-activated estrogen receptor {alpha} (ER{alpha}) and ß (ERß) are able to induce transcriptional activation of signal transducer and activator of transcription (Stat)-regulated promoters via cytoplasmic signal transduction pathways. Stat5 and Stat3 are required for promoter induction, which correlates with cytoplasmic sublocalization of ERs and is independent of intact coactivator binding sites and DNA-binding domains. In endothelial cells, Stat5 and Stat3 are rapidly phosphorylated on both tyrosine and serine residues in response to 17ß-estradiol, and nuclear translocation is subsequently induced. 17ß-Estradiol-induced transactivation of a Stat-regulated promoter requires at least three different signal transduction pathways, including MAPK, Src-kinase, and phosphatidylinositol-3-kinase activities. In conclusion, this work identifies a novel pathway involving an agonist-bound ER-activated phosphorylation cascade, resulting in nuclear transcriptional activation of target transcription factors. These findings reveal novel targets for the development of drugs that modulate a nongenomic-to-genomic ER-dependent mechanism.

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα  |  ERβ
Ligands:   17β-Estradiol  |  4-Hydroxytamoxifen  |  Raloxifene



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