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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0094v1 200/3/311    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Müller, P. Articles by Ström, A. Search for Related Content PubMed PubMed Citation Articles by Müller, P. Articles by Ström, A.

¹ Department of Biosciences and Nutrition, Karolinska Institutet, Novum, S-141 57 Huddinge, Sweden² Department of Microbiology and Molecular Biology, Brigham Young University, Provo, Utah 84602, USA

(Correspondence should be addressed to A Ström; Email: anders.strom{at}ki.se)

Regulation of hairy and enhancer of split homologue-1 (HES-1) by estradiol and all-trans retinoic acid affects proliferation of human breast cancer cells. Here, we identify and characterize cis-regulatory elements involved in HES-1 regulation. In the distal 5' promoter of the HES-1 gene, we found a retinoic acid response element and in the distal 3' region, an estrogen receptor (ER) binding site. The ER binding site, composed of an estrogen response element (ERE) and an ERE half-site, is important for both ER binding and transcriptional regulation. Chromatin immunoprecipitation assays revealed that ER is recruited to the ERE and associates with the HES-1 promoter. We also show recruitment of nuclear receptor co-regulators to the ERE in response to estradiol, followed by a decrease in histone acetylation and RNA polymerase II docking in the HES-1 promoter region. Our findings are consistent with a novel type of repressive estrogen response element in the distal 3' region of the HES-1 gene.