M. Schulz, M. Eggert, A. Baniahmad, A. Dostert, T. Heinzel and R. Renkawitz, “RU486-Induced Glucocorticoid Receptor Agonism Is Controlled by the Receptor N Terminus and by Corepressor Binding,” Journal of Biological Chemistry, Vol. 277, No. 29, 2002, pp. 26238-26243. doi:10.1074/jbc.M203268200

has been cited by the following article:

• TITLE: RU486 Reversal of Cortisol Repression of 1,25-Dihydroxyvitamin D3 Induction of the Human Osteocalcin Promoter

  AUTHORS: Nigel A. Morrison

  KEYWORDS: RU486; Osteocalcin; Vitamin D; Glucocorticoid

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.1, February 25, 2013

  ABSTRACT: In conditions of corticosteroid excess, such as Cushing’s syndrome, a reduction in serum osteocalcin is observed and bone loss occurs. The human osteocalcin gene is induced by 1,25-dihydroxyvitamin D3 derivatives and repressed by glucocorticoids. In this paper we show that cortisol, a natural glucocorticoid, represses both basal and vitamin D induced activity of the human osteocalcin promoter. Furthermore, we address the specific question as to whether the anti-progestin anti-glucocorticoid RU486 is able to antagonize the inhibitory effect of cortisol on osteocalcin gene expression. We show that RU486 has agonist activity alone, in that it is able to repress the basal promoter activity of the osteocalcin gene and antagonist activity, reversing incompletely the cortisol mediated repression of 1,25-dihydroxyvitamin D3 induction.