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Brüning, J.C. et al.

Brüning, Lingohr, Gillette, Hanstein, Avci, Krone, Müller-Wieland, Kotzka,

Estrogen receptor-alpha and Sp1 interact in the induction of the low density lipoprotein-receptor.

Both estrogen and selective estrogen receptor modulators (SERMs) such as tamoxifen and raloxifene have been demonstrated to lower plasma low density lipoprotein (LDL)-cholesterol concentrations by stimulation of LDL receptor gene expression. To determine the molecular mechanisms of estradiol- and tamoxifen-induced LDL receptor expression, we performed transient transfection experiments with luciferase reporter gene-constructs under transcriptional control of the human LDL receptor promoter. We demonstrate, that estradiol and tamoxifen stimulate LDL receptor gene expression in human HepG2 hepatoma cells only when estrogen receptor (ER)-alpha but not when ER-beta is cotransfected. Deletion mutants and point mutations of the LDL receptor promoter reveal that estradiol- and tamoxifen-stimulated expression of this gene depends on an intact repeat 3 in the LDL receptor promoter, a cis-element previously shown to interact with Sp1. Gel mobility analyses demonstrated estradiol- and tamoxifen-stimulated binding of nuclear proteins to repeat 3 (bp -56 to bp -36) of the LDL receptor promoter. These data provide an alternative mechanism of LDL receptor gene expression by non-classical estradiol- and tamoxifen- stimulated induction through an ER-alpha/Sp1 complex.[1]

References

Estrogen receptor-alpha and Sp1 interact in the induction of the low density lipoprotein-receptor. Brüning, J.C., Lingohr, P., Gillette, J., Hanstein, B., Avci, H., Krone, W., Müller-Wieland, D., Kotzka, J. J. Steroid Biochem. Mol. Biol. (2003) [Pubmed]

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