Relationship between receptor and mammary tumour virus production after stimulation by glucocorticoid.
A short exposure of primary cultures of mouse mammary tumour cells to glucocorticoids results in at least a three-fold stimulation of mammary tumour virus (MTV) production. Specific interaction of glucocorticoids with the cytoplasmic and nuclear receptors can also be demonstrated. The biological potency of various steroids to stimulate MTV is related directly to the retention of the steroid-receptor complex in the nuclei. Progesterone has a high affinity for the cytoplasmic receptor, is not retained by the nuclei and does not stimulate or block the basal level of MTV production. It is, however, quite effective in abolishing the glucocorticoid-mediated stimulation of MTV and thus behaves as an antagonist of glucocorticoid.
D000818:Animals; D001667:Binding, Competitive; D002467:Cell Nucleus / Q000378:metabolism; D002478:Cells, Cultured; D003593:Cytoplasm / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism / Q000494:pharmacology; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism / Q000382:microbiology; D008324:Mammary Tumor Virus, Mouse / Q000254:growth & development*; D011374:Progesterone / Q000378:metabolism / Q000494:pharmacology; D011956:Receptors, Cell Surface; D014779:Virus Replication / Q000187:drug effects*
D005938:Glucocorticoids; D011956:Receptors, Cell Surface; D011374:Progesterone; D003907:Dexamethasone