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Nuclear Receptor Signaling Atlas
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NR3C2
Overview
Synonyms
LOC100534796 ; MCR ; MLR ; MR ; Mineralocorticoid receptor (aldosterone receptor) ; Mlr ; NR3C2 ; NR3C2VIT ; Nr3c2 ; aldosterone receptor ; mineralocorticoid receptor ; mineralocorticoid receptor 1 ; mineralocorticoid receptor delta ; nuclear receptor subfamily 3 group C member 2
NURSA Name
Mineralocorticoid receptor
Official Symbol
NR3C2
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Description
The MR is a mineralocorticoid and glucocorticoid-activated steroid receptor member of the nuclear receptor superfamily of transcription factors. It plays a critical role in regulating electrolyte and fluid balance in the kidney, as well as having specific roles in the central nervous system (CNS). MR is expressed at moderate levels in tissues in all major physiological systems (central nervous system (CNS), endocrine, metabolic, gastrointestinal, immune, reproductive, cardiovascular, respiratory and structural) with particularly high levels in the brain stem, cerebellum, colon, prostate and skin. MR dysfunction has been associated with metabolic disorders (pseudohypoaldosteronism), cardiovascular defects (hypertension), psychiatric disorders (depression, stress) and reproductive conditions (preeclampsia). Targeted deletion (knockout) of MR results in pseudohypoaldosteronism, hyperkalemia, hyponatremia and a strong increase in plasma concentrations of renin, angiotenisin II and aldosterone. Death occurs from dehydration through sodium and water loss. Floxed deletion of MR in the limbic system results in impaired behavioral plasticity.
Original References:
Arriza JL, Weinberger C, Cerelli G, Glaser TM, Handelin BL, Housman DE and Evans RM (1987) Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor. Science 237 268-75 View Abstract | View PubMed
Zennaro MC, Souque A, Viengchareun S, Poisson E and Lombès M (2001) A new human MR splice variant is a ligand-independent transactivator modulating corticosteroid action. Mol. Endocrinol. 15 1586-98 View Abstract | View PubMed
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