Figure 2.

Scheme of the complex hormonal balance in the control of RACK1 expression. Data suggest that cortisol and dehydroepiandrosterone (DHEA) can influence alternative splicing of the GR, controlling the level of exon inclusion/exclusion in the mRNA transcript [17,18], and therefore suggesting that the anti-glucocorticoid effect of DHEA is due, in part, to modulation of the expression of proteins involved in the splicing of the glucocorticoid receptor (GR) pre-mRNA. In addition, the effect of DHEA on RACK1 expression is dependent on its transformation into active androgen steroids [52]. Although pharmacological evidence supports the role of the AR, there is not yet direct demonstration of the interaction of the androgen receptor (AR) with the hormone sensitive site on the rack1 gene promoter; hence the dotted line arrow in the scheme.