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Data demonstrate that there are distinct differences between the human mineralocorticoid receptor (MR) and the zebrafish MR despite considerable sequence and functional conservation.
SUMOylation of 11beta-HSD2 (show HSD11B2 Proteins) at residue K266 modulates cortisol-mediated MR nuclear translocation independently of effects on transactivation.
haplotype TAAT of GR might be a protective factor against aggressive behavior, while gene-gene interactions between GR (NR3C1 (show NR3C1 Proteins)) rs1800445 and MR (NR3C2) rs2070951 might be a risk factor for aggressive behavior in the Central South Chinese Han population
Polymorphisms of the glucocorticoid receptor (show NR3C1 Proteins) gene influenced both the basal state of the hypothalamus-pituitary-adrenal axis as well as self-perceived stress. The mineralocorticoid receptor gene only associated with self-perceived stress and 5-HTT (show SLC6A4 Proteins) only with the cortisol awakening response.
Low NR3C2 expression is associated with Pancreatic Cancer.
the variant rs2070951 and the GA haplotype in NR3C2 were associated with an increased risk for cCSC. Results of this genetic study support a possible role for the mineralocorticoid receptor in the pathogenesis of cCSC.
Glucocorticoid receptor (GR (show NR3C1 Proteins)) and Mineralocorticoid Receptor (MR) actions on NFkappaB (show NFKB1 Proteins) - and AP-1 (show FOSB Proteins)-dependent signaling were compared in a standardized cellular context where GR or MR could be specifically expressed in the absence of other nuclear receptors. Like GR, MR was found to repress NFkappaB (show NFKB1 Proteins)-driven transcription in these cells.
The new frameshift mutation decreased the expression of MR, but not NR3C2 mRNA, and led to decreased MR function, with no dominant negative effect.
dysregulation of GR, MR, FKBP5 (show FKBP5 Proteins), and PTGES3 (show PTGES3 Proteins) in autistic spectrum disorder (ASD (show ARSD Proteins)) and suggest a possible role of inflammation in altered GR function in ASD (show ARSD Proteins).
hyperactive hypothalamo-pituitary-adrenocortical axis in overweight diabetic subjects may be associated with downregulation of 11beta-HSD1 (show HSD11B1 Proteins), MR, and GR in the brain.
Our current findings demonstrate that Arctigenin is an antagonist of MR and effectively decreases the Na/K-ATPase 1 (show ATP1A1 Proteins) gene expression. Our work provides a hint for the drug discovery against cardiovascular disease
myeloid MR knockout (MRKO) improves glucose intolerance, insulin (show INS Proteins) resistance, and hepatic steatosis in obese mice. Estrogen signaling is sufficient and necessary for such improvements. Hepatic gene and protein expression suggests that MRKO reduces hepatic lipogenesis and lipid storage.
Nr3c2 has a role in mouse skin development in a process that involves HSD11B1 (show HSD11B1 Proteins)/HSD11B2 (show HSD11B2 Proteins)
Inducible Knock-Down of the Mineralocorticoid Receptor in Mice Disturbs Regulation of the Renin (show REN Proteins)-Angiotensin-Aldosterone System and Attenuates Heart Failure Induced by Pressure Overload
Data indicate that endothelial cell mineralocorticoid receptor (MR) deficiency prevented Western diet (WD)-induced diastolic dysfunction, profibrotic, and progrowth signaling.
Cardiomyocyte mineralocorticoid receptor activation impairs acute cardiac functional recovery after ischemic insult.
a cooperative role of MR and cav-1 (show CAV1 Proteins) in regulating vascular contraction and NO-cGMP-mediated relaxation during low NO-high AngII-dependent cardiovascular injury
Upregulation of MR in mouse adipocytes led to increased weight and fat mass, insulin (show INS Proteins) resistance, and metabolic syndrome features without affecting blood pressure.
Data showed that the mRNA expression of glucocorticoid and mineralocorticoid receptors were significantly decreased in splenic macrophages by repeated social defeat. Epigenetic regulation, may play a role in the RSD-induced GC resistance.
Compared to sham-mice, the expression levels of hypothalamic MR, serum glucocorticoid-induced kinase 1 (a marker of MR activity) and AT1R (show AGTRAP Proteins) increased in pressure-overload-mice.
Data indicate that overexpression of constitutively active Rac1 activated mineralocorticoid receptor (MR).
This gene encodes the mineralocorticoid receptor, which mediates aldosterone actions on salt and water balance within restricted target cells. The protein functions as a ligand-dependent transcription factor that binds to mineralocorticoid response elements in order to transactivate target genes. Mutations in this gene cause autosomal dominant pseudohypoaldosteronism type I, a disorder characterized by urinary salt wasting. Defects in this gene are also associated with early onset hypertension with severe exacerbation in pregnancy. Alternative splicing results in multiple transcript variants.
, nuclear receptor subfamily 3, group C, member 2
, nuclear receptor subfamily 3 group C member 2
, aldosterone receptor
, mineralocorticoid receptor 1
, mineralocorticoid receptor delta
, Mineralocorticoid receptor (aldosterone receptor)