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Corticosteroid receptors refer collectively to two closely related members of the nuclear hormone receptor superfamily: the **glucocorticoid receptor** and **mineralocorticoid receptor**. Both are intracellular transcription factors that bind steroid hormones produced by the adrenal cortex—primarily cortisol/corticosterone for GR and aldosterone/corticosterone for MR. Upon ligand binding in the cytoplasm, they undergo conformational change allowing translocation into the nucleus where they regulate gene expression by binding specific DNA sequences known as glucocorticoid or mineralocorticoid response elements. These actions mediate diverse physiological processes including immune modulation, metabolism regulation, stress adaptation, electrolyte balance—and underlie their therapeutic use in inflammatory diseases while also accounting for their wide-ranging side effects.[1][3][4] The term "corticosteroid receptors" is not a precise molecular designation but rather an umbrella term encompassing both glucocorticoid and mineralocorticoid receptors.[1]
Drugs act as agonists or antagonists at these nuclear receptors. Upon ligand binding in the cytoplasm, - The activated complex translocates to the nucleus, - Binds specific DNA response elements, - Modulates transcription of target genes. Mechanisms include both direct gene activation/repression and interference with other transcription factors such as NF-kB/AP1 ("transactivation" and "transrepression")
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