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This version published online on July 11, 2002
Molecular Endocrinology, doi:10.1210/me.2002-0072
Molecular Endocrinology Vol. 0, No. 2002 200200721-
doi:10.1210/me.2002-0072
Copyright © 2002 by the Endocrine Society.
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Submitted on February 18, 2002
Accepted on June 24, 2002

STATs as Downstream Targets of Non-Genomic Estrogen Receptor Actions

Linda Björnström1 and Maria Sjöberg1*

1 Dept. of Cell and Molecular Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden

* To whom correspondence should be addressed. 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 sublocalisation of ERs and is independent of intact co-activator 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 MAP-kinase, Src-kinase and PI3-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 non-genomic to genomic ER-dependent mechanism.
Key words: estrogen receptor • MAP-kinase • non-genomic • signal transduction • STAT

NURSA Molecule Pages Link:

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



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