Funder J W
Baker Medical Research Institute, Prahran, Australia.
Annu Rev Med. 1997;48:231-40. doi: 10.1146/annurev.med.48.1.231.
Mineralocorticoid and glucocorticoid receptors act as homodimers via canonical pentadecamer hormone response elements to regulate transcription. Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown also to modulate AP-1- and NF kappa B-induced transcription by direct protein-protein interactions. The role of 11 beta-hydroxysteroid dehydrogenase in conferring aldosterone specificity on epithelial mineralocorticoid receptors has been proven by the demonstration of sequence mutations in all cases of apparent mineralocorticoid excess examined to date. The autosomal form of aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect loss-of-function mutations in epithelial sodium channel subunit sequence. (Patho)physiological roles for aldosterone and glucocorticoid membrane receptors, and for the recently described nuclear receptors for 11-ketosteroids in 11 beta-hydroxysteroid dehydro-genase-protected epithelia, remain to be established.
盐皮质激素和糖皮质激素受体通过典型的十五聚体激素反应元件作为同二聚体发挥作用，以调节转录。糖皮质激素受体（而非盐皮质激素受体）已被证明还可通过直接的蛋白质-蛋白质相互作用来调节AP-1和NF-κB诱导的转录。通过对迄今为止检查的所有明显盐皮质激素过多病例中的序列突变进行论证，已证实11β-羟类固醇脱氢酶在赋予上皮盐皮质激素受体醛固酮特异性方面的作用。常染色体形式的醛固酮抵抗（假性醛固酮增多症）已被证明反映了上皮钠通道亚基序列中的功能丧失突变。醛固酮和糖皮质激素膜受体以及最近在11β-羟类固醇脱氢酶保护的上皮细胞中描述的11-酮类固醇核受体的（病理）生理作用仍有待确定。
