Abstract
Four antiglucocorticoids, RU38486, RU5020, RU25055 and progesterone were found to antagonize the induction of latent Epstein-Barr virus (EBV) information by dexamethasone. The dose-response studies show that the antagonization was more prominent with the synthetic steroids than with the natural hormone. Specific binding characteristics of dexamethasone measured in whole cells indicate the presence of glucocorticoid receptors. Total cellular receptor contents deduced from binding data give values similar to those reported for B-lymphoblasts. Competition experiments between dexamethasone and RU38436 strongly suggest that RU38486 binds to two distinct sites in the whole cell; one is the glucocorticoid receptor but the nature of the other site is unknown. Inhibition by antiglucocorticoids differs from antagonism by 12- O-tetradecanoyl-phorbol-13-acetate (TPA) since the latter does not compete for any sites interacting with RU38486.
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