Alternative splicing of the human glucocorticoid receptor gene generates a nonhormone
binding splice variant (hGRβ) that differs from the wild-type receptor (hGRα) only at the
carboxyl terminus. Previously we have shown that hGRβ inhibits the transcriptional activity of
hGRα, which is consistent with reports of elevated hGRβ expression in patients with
generalized and tissue-specific glucocorticoid resistance. The potential role of hGRβ in the
regulation of target cell sensitivity to glucocorticoids prompted us to further evaluate its …