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Signaling and Regulation

Interaction between Transcription Factor, Basal Transcription Factor 3, and the NH₂-Terminal Domain of Human Estrogen Receptor

¹ Queen's University Belfast, Centre of Cancer Research and Cell Biology, Belfast City Hospital, Belfast, United Kingdom; ² University of Ulster, Coleraine, Londonderry, United Kingdom; and ³ School of Biological Sciences, University of Liverpool, Liverpool, United Kingdom

Requests for reprints: Mohamed K. El-Tanani, Centre for Cancer Research and Cell Biology, Queen's University Belfast, University Floor, Belfast City Hospital, Lisburn Road, Belfast BT9 7AB, United Kingdom. Phone: 44-28-9026-3486; Fax: 44-9026-3744. E-mail: m.el-tanani{at}qub.ac.uk

The estrogen receptor (ER), like other members of the nuclear receptor superfamily, possesses two separate transcriptional activation functions, AF-1 and AF-2. Although a variety of coactivators and corepressors of AF-2 have been identified, less is known of the mechanism of action of AF-1. We have used the yeast two-hybrid system to isolate a cDNA coding for a protein that binds specifically to the AF-1 region of human ER. This cDNA codes for the transcription factor basal transcription factor 3 (BTF3). The specificity of the interaction between BTF3 and ER has been confirmed in vivo and in vitro. Transient transfection experiments reveal that overexpression of BTF3 modulates the transcriptional response of reporter genes to ER. BTF3 interacts with ER that has been activated either by 17ß-estradiol (ligand-dependent activation) or by epidermal growth factor (ligand-independent activation). The effects of BTF3 on the reporter genes requires the presence of ER containing an active AF-1 function. BTF3 may be a component of the mechanism by which the AF-1 function of ER stimulates gene transcription. (Mol Cancer Res 2007;5(11):1191–200)