Studies on the translocation inhibitor of 3H-dexamethasone-receptor complex.
Recent reports on the binding of glucocorticoid-receptor complexes to rat liver nuclei suggested the presence of components which inhibited the binding. The inhibitory component(s) of the receptor translocation was observed not only in the cytosol of the liver but also in cytosols of the kidney, the spleen and the thymus. The cytoplasmic levels of the inhibitor in these tissues were not modified by the administration of Dexamthasone (DEX). The liver inhibitor was macromolecular and clearly separated from the DEX-receptor complex on DEAE-cellulose chromatography. The mechanism of the inhibition seemed to be an interaction between the inhibitor and the steroid-receptor complex. In addition, the inhibition seemed to be less specific for the bindings of different steroid-receptor complexes to nuclei. The bindings of hepatic 3H-DEX-receptor complex by nuclei derived from livers of adrenalectomized and DEX-treated rats, in the presence or absence of the translocation inhibitor, were similar.
D000315:Adrenalectomy; D000818:Animals; D002848:Chromatography, DEAE-Cellulose; D003600:Cytosol / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D014316:Tritium
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D014316:Tritium; D003907:Dexamethasone