Mineralocorticoid response element

Funder, J. W., Mineralocorticoids, glucocorticoids, receptors and response elements. Science 259 1132-1133, 1993. 

Fig. 5. Specificity of steroid response element. A. In this example (mouse mammary tumour virus), the element will bind receptors for glucocorticoids (G), androgen (A), progestin (P) and mineralocorticoid (M) so that each of these classes of steroid stimulate transcription. This type of specificity can vary from cell to cell possibly due to other protein factors (not shown). B. Although oestrogen (E) receptor will not act as an agonist for mouse mammary tumour virus transcription, it may antagonise the agonist activity of glucocorticoids (G).

The steroid receptor family inclndes androgen receptors (AR), estrogen receptors (ER, a. and (3), progesterone receptors (PR, A and B), glncocorticoid receptors (GR), and mineralocorticoid receptors (MR). Traditional models propose that, upon binding their hormonal ligand, the receptors release heat shock proteins like hsp90, translocate into the nucleus, and bind as homodimers to imperfect palindromic response elements at upstream promoter sites. 

The steroid receptor superfamily comprises the glucocorticoid (GR), progesterone (PR), mineralocorticoid (MR), androgen (AR), thyroid hormone (TR),and vitamin Dg (VDR) receptors (60). These receptors bind to steroid hormones and are translocated to the nucleus where they bind to hormone responsive elements on DNA promoter regions to alter gene expression. While steroids are very effective anti-inflammatory agents, they have a multiplicity of serious side effects that limit their full use. 

A. Mechanism of Action Corticosteroids enter the cell and bind to cytosolic receptors that transport the steroid into the nucleus. The steroid-receptor complex alters gene expression by binding to glucocorticoid response elements (GREs) or mineralocorticoid-specific elements (Figure 39-2). Tissue-specific responses to steroids are made possible by the presence in each tissue of different protein regulators that control the interaction between the hormone-receptor complex and particular response elements. 

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