PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17683282-4 2007 The MR may be activated by aldosterone and cortisol or via transactivation by the AT(1) (angiotenin II type 1) receptor through a mechanism involving the EGFR (epidermal growth factor receptor) and MAPK (mitogen-activated protein kinase) pathway. Hydrocortisone 43-51 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 17666187-4 2007 Herein, we propose that an MR agonist may inhibit the HPA axis without first "unloading" receptors of endogenous cortisol. Hydrocortisone 113-121 nuclear receptor subfamily 3 group C member 2 Homo sapiens 27-29 20409908-5 2008 In high/normal renin hypertensives, the elevated 11beta-HSD2-GALFs may have two major functions: increased Na(+) retention by the kidney by allowing cortisol to access the renal mineralocorticoid receptor and increased vascular reactivity by allowing cortisol to access the vascular mineralocorticoid receptor. Hydrocortisone 149-157 nuclear receptor subfamily 3 group C member 2 Homo sapiens 178-204 17035606-1 2006 In mineralocorticoid target tissues such as the cortical collecting duct in the kidney, the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is responsible for the peripheral inactivation of cortisol to cortisone, thereby protecting the mineralocorticoid receptor from inappropriate activation by cortisol. Hydrocortisone 205-213 nuclear receptor subfamily 3 group C member 2 Homo sapiens 251-277 17035606-1 2006 In mineralocorticoid target tissues such as the cortical collecting duct in the kidney, the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is responsible for the peripheral inactivation of cortisol to cortisone, thereby protecting the mineralocorticoid receptor from inappropriate activation by cortisol. Hydrocortisone 311-319 nuclear receptor subfamily 3 group C member 2 Homo sapiens 251-277 19804189-3 2006 In all three trials, plasma aldosterone levels were low and sodium status unremarkable; this finding, and those of various preclinical studies, point squarely at pathophysiological MR activation by ligands other than aldosterone, most likely normal levels of cortisol, and provide clear evidence for the therapeutic utility of MR blockade in conditions of tissue and organ damage with normal aldosterone levels. Hydrocortisone 259-267 nuclear receptor subfamily 3 group C member 2 Homo sapiens 181-183 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 90-98 nuclear receptor subfamily 3 group C member 2 Homo sapiens 44-70 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 90-98 nuclear receptor subfamily 3 group C member 2 Homo sapiens 72-74 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 90-98 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-200 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 232-240 nuclear receptor subfamily 3 group C member 2 Homo sapiens 44-70 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 232-240 nuclear receptor subfamily 3 group C member 2 Homo sapiens 72-74 17006915-4 2006 The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. Hydrocortisone 232-240 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-200 15643127-1 2005 BACKGROUND: The 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) catalyzes the conversion of cortisol (F) to cortisone (E), avoiding the interaction of cortisol with the mineralocorticoid receptor. Hydrocortisone 100-108 nuclear receptor subfamily 3 group C member 2 Homo sapiens 177-203 15761029-3 2005 We also discovered that cortisol, the preferred physiological ligand for the glucocorticoid receptor in humans, is a partial MR agonist/antagonist, providing a possible molecular explanation of the tissue-selective effects of glucocorticoids on MR. Hydrocortisone 24-32 nuclear receptor subfamily 3 group C member 2 Homo sapiens 125-127 15761029-3 2005 We also discovered that cortisol, the preferred physiological ligand for the glucocorticoid receptor in humans, is a partial MR agonist/antagonist, providing a possible molecular explanation of the tissue-selective effects of glucocorticoids on MR. Hydrocortisone 24-32 nuclear receptor subfamily 3 group C member 2 Homo sapiens 245-247 15761029-4 2005 However, when we examined the coactivator and corepressor peptide interactions in the presence of cortisol, we found that MR bound with cortisol or aldosterone interacted with the same set of peptides. Hydrocortisone 98-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 122-124 15761029-4 2005 However, when we examined the coactivator and corepressor peptide interactions in the presence of cortisol, we found that MR bound with cortisol or aldosterone interacted with the same set of peptides. Hydrocortisone 136-144 nuclear receptor subfamily 3 group C member 2 Homo sapiens 122-124 15761029-7 2005 In addition, we also show that cortisol becomes full agonist when S810L mutation is introduced in the LBD of MR. Hydrocortisone 31-39 nuclear receptor subfamily 3 group C member 2 Homo sapiens 109-111 15860254-5 2005 In these instances, there is increasing evidence that coronary and cardiac MR are activated by normal circulating cortisol levels, in the cellular context of generation of reactive oxygen species (ROS) and/or alteration in intracellular redox status. Hydrocortisone 114-122 nuclear receptor subfamily 3 group C member 2 Homo sapiens 75-77 15860254-6 2005 MR in VSMC and cardiomyocytes are normally predominantly occupied by cortisol in tonic inhibitory mode. Hydrocortisone 69-77 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2 16980198-5 2006 By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the mineralocorticoid receptor (MR) by cortisol. Hydrocortisone 139-147 nuclear receptor subfamily 3 group C member 2 Homo sapiens 191-217 16980198-5 2006 By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the mineralocorticoid receptor (MR) by cortisol. Hydrocortisone 139-147 nuclear receptor subfamily 3 group C member 2 Homo sapiens 219-221 16980198-5 2006 By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the mineralocorticoid receptor (MR) by cortisol. Hydrocortisone 226-234 nuclear receptor subfamily 3 group C member 2 Homo sapiens 191-217 16868910-4 2006 Apparent Mineralocorticoid Excess (AME) is due to a mutation of the gene encoding the renal isoform of 11 a HSD enzyme; the non-conversion of cortisol to cortisone result in increasing cortisol levels that activate the mineralocorticoid receptor. Hydrocortisone 142-150 nuclear receptor subfamily 3 group C member 2 Homo sapiens 219-245 16868910-4 2006 Apparent Mineralocorticoid Excess (AME) is due to a mutation of the gene encoding the renal isoform of 11 a HSD enzyme; the non-conversion of cortisol to cortisone result in increasing cortisol levels that activate the mineralocorticoid receptor. Hydrocortisone 185-193 nuclear receptor subfamily 3 group C member 2 Homo sapiens 219-245 16778331-2 2006 In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Hydrocortisone 111-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-102 16778331-2 2006 In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Hydrocortisone 111-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 104-106 15967794-6 2005 Taken together, these results explain the potency of MR activation by aldosterone, the weak activation induced by progesterone and the antihypertensive agent spironolactone, and the binding selectivity of cortisol over cortisone. Hydrocortisone 205-213 nuclear receptor subfamily 3 group C member 2 Homo sapiens 53-55 15761540-2 2004 This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol (F) to its inactive metabolite cortisone (E). Hydrocortisone 96-104 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-63 15761540-2 2004 This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol (F) to its inactive metabolite cortisone (E). Hydrocortisone 96-104 nuclear receptor subfamily 3 group C member 2 Homo sapiens 65-67 15134813-1 2004 11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays a crucial role in converting hormonally active cortisol to inactive cortisone, thereby conferring specificity upon the mineralocorticoid receptor (MR). Hydrocortisone 110-118 nuclear receptor subfamily 3 group C member 2 Homo sapiens 182-208 15241728-1 2004 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays a crucial role in converting hormonally active cortisol into inactive cortisone, conferring specificity onto the human mineralocorticoid receptor (MR). Hydrocortisone 110-118 nuclear receptor subfamily 3 group C member 2 Homo sapiens 182-208 15241728-1 2004 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays a crucial role in converting hormonally active cortisol into inactive cortisone, conferring specificity onto the human mineralocorticoid receptor (MR). Hydrocortisone 110-118 nuclear receptor subfamily 3 group C member 2 Homo sapiens 210-212 14741058-3 2004 A recent study showed that blocking brain MR activity not only enhances CRF-induced ACTH and cortisol release, but also significantly reduces SWS in humans. Hydrocortisone 93-101 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-44 15134813-1 2004 11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays a crucial role in converting hormonally active cortisol to inactive cortisone, thereby conferring specificity upon the mineralocorticoid receptor (MR). Hydrocortisone 110-118 nuclear receptor subfamily 3 group C member 2 Homo sapiens 210-212 15134814-2 2004 MR binds aldosterone and physiologic glucocorticoids, such as cortisol, which both can act as MR agonists in epithelial tissues. Hydrocortisone 62-70 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2 15134814-2 2004 MR binds aldosterone and physiologic glucocorticoids, such as cortisol, which both can act as MR agonists in epithelial tissues. Hydrocortisone 62-70 nuclear receptor subfamily 3 group C member 2 Homo sapiens 94-96 12852254-7 2003 In some of these disorders, mineralocorticoid hypertension results from activation of the mineralocorticoid receptor by other steroids (cortisol, deoxycorticosterone), by primary activation of the receptor itself, or by constitutive overactivity of the renal epithelial sodium channel. Hydrocortisone 136-144 nuclear receptor subfamily 3 group C member 2 Homo sapiens 90-116 14614041-1 2003 In mineralocorticoid target tissues, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) confers mineralocorticoid receptor selectivity by metabolizing hormonally active cortisol to inactive cortisone, allowing aldosterone access to the receptor. Hydrocortisone 175-183 nuclear receptor subfamily 3 group C member 2 Homo sapiens 102-128 12644298-10 2003 Interestingly, cortisol produces a much weaker N/C-interaction than aldosterone, and it is possible that the N/C-interaction may contribute to observed functional differences in the MR bound to the two ligands. Hydrocortisone 15-23 nuclear receptor subfamily 3 group C member 2 Homo sapiens 182-184 14608520-5 2003 MR blockade is, however, effective both in situations with and without an increase in serum aldosterone level, since the MR can be occupied and activated by cortisol as well as by aldosterone. Hydrocortisone 157-165 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2 14608520-5 2003 MR blockade is, however, effective both in situations with and without an increase in serum aldosterone level, since the MR can be occupied and activated by cortisol as well as by aldosterone. Hydrocortisone 157-165 nuclear receptor subfamily 3 group C member 2 Homo sapiens 121-123 12788846-1 2003 The human microsomal 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) metabolizes active cortisol into cortisone and protects the mineralocorticoid receptor from glucocorticoid occupancy. Hydrocortisone 99-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 140-166 12788846-2 2003 In a congenital deficiency of 11 beta-HSD2, the protective mechanism fails and cortisol gains inappropriate access to mineralocorticoid receptor, resulting in low-renin hypertension and hypokalemia. Hydrocortisone 79-87 nuclear receptor subfamily 3 group C member 2 Homo sapiens 118-144 12711009-1 2003 The mineralocorticoid receptor (MR) binds aldosterone, but also glucocorticoid hormones (corticosterone in rodents, cortisol in humans), which largely prevail in the plasma. Hydrocortisone 116-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 12711009-1 2003 The mineralocorticoid receptor (MR) binds aldosterone, but also glucocorticoid hormones (corticosterone in rodents, cortisol in humans), which largely prevail in the plasma. Hydrocortisone 116-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 12015312-0 2002 Chenodeoxycholic acid and deoxycholic acid inhibit 11 beta-hydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor. Hydrocortisone 105-113 nuclear receptor subfamily 3 group C member 2 Homo sapiens 156-182 12587501-3 2002 This enzyme catalyzes the conversion of cortisol to cortisone, avoiding the interaction of cortisol with the mineralocorticoid receptor. Hydrocortisone 40-48 nuclear receptor subfamily 3 group C member 2 Homo sapiens 109-135 11502780-6 2001 The case also demonstrates the potential need for concomitant mineralocorticoid receptor blockade in mifepristone-treated Cushing"s disease, because cortisol levels may rise markedly, reflecting corticotroph disinhibition, to cause manifestations of mineralocorticoid excess. Hydrocortisone 149-157 nuclear receptor subfamily 3 group C member 2 Homo sapiens 62-88 11576621-1 2001 OBJECTIVE: The conversion of cortisol, which binds avidly to the mineralocorticoid receptor, to cortisone, which no longer has mineralocorticoid function, is predominantly catalyzed by the 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD 2). Hydrocortisone 29-37 nuclear receptor subfamily 3 group C member 2 Homo sapiens 65-91 10726708-1 2000 The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans. Hydrocortisone 240-248 nuclear receptor subfamily 3 group C member 2 Homo sapiens 189-215 11114699-1 2000 The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11BHSD2) converts cortisol to cortisone in the kidney, thereby protecting the mineralocorticoid receptor from the mineralocorticoid actions of cortisol. Hydrocortisone 74-82 nuclear receptor subfamily 3 group C member 2 Homo sapiens 134-160 11114699-1 2000 The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11BHSD2) converts cortisol to cortisone in the kidney, thereby protecting the mineralocorticoid receptor from the mineralocorticoid actions of cortisol. Hydrocortisone 199-207 nuclear receptor subfamily 3 group C member 2 Homo sapiens 134-160 11005270-2 2000 This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol to its inactive metabolite cortisone. Hydrocortisone 96-104 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-63 11005270-2 2000 This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol to its inactive metabolite cortisone. Hydrocortisone 96-104 nuclear receptor subfamily 3 group C member 2 Homo sapiens 65-67 11740142-11 2001 (b) AME is caused by mutations of the 11beta-hydroxysteroid dehydrogenase type 2 enzyme, an enzyme that metabolizes cortisol into its receptor inactive keto-form cortisone, thus protecting the mineralocorticoid receptor (MR) from occupation by glucocorticoids. Hydrocortisone 116-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 193-219 11740142-11 2001 (b) AME is caused by mutations of the 11beta-hydroxysteroid dehydrogenase type 2 enzyme, an enzyme that metabolizes cortisol into its receptor inactive keto-form cortisone, thus protecting the mineralocorticoid receptor (MR) from occupation by glucocorticoids. Hydrocortisone 116-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 221-223 10726708-1 2000 The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans. Hydrocortisone 240-248 nuclear receptor subfamily 3 group C member 2 Homo sapiens 217-219 10726708-2 2000 Inhibition by xenobiotics such as liquorice or mutations in the HSD11 B2 gene, as occur in the rare monogenic hypertensive syndrome of apparent mineralocorticoid excess (AME), result in a compromised 11 betaHSD2 enzyme activity, which in turn leads to overstimulation of the MR by cortisol, sodium retention, hypokalaemia, low plasma renin and aldosterone concentrations, and hypertension. Hydrocortisone 281-289 nuclear receptor subfamily 3 group C member 2 Homo sapiens 275-277 9029719-13 1997 The demonstration of a nuclear localization for what was thought to be principally a microsomal enzyme suggests that interaction between the MR and its ligand (either aldosterone or cortisol) may be a nuclear rather than a cytoplasmic event. Hydrocortisone 182-190 nuclear receptor subfamily 3 group C member 2 Homo sapiens 141-143 10620097-3 1999 This enzyme catalyses the interconversion between cortisol and cortisone and normally protects the mineralocorticoid receptor from being activated by cortisol. Hydrocortisone 50-58 nuclear receptor subfamily 3 group C member 2 Homo sapiens 99-125 10620097-3 1999 This enzyme catalyses the interconversion between cortisol and cortisone and normally protects the mineralocorticoid receptor from being activated by cortisol. Hydrocortisone 150-158 nuclear receptor subfamily 3 group C member 2 Homo sapiens 99-125 10620097-16 1999 This is caused by 18betaGA-mediated inhibition of 11betaHSD, resulting in activation of the renal mineralocorticoid receptor by cortisol. Hydrocortisone 128-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 98-124 10689617-5 1999 The MR model allowed the identification of several residues involved in the interaction with aldosterone and cortisol. Hydrocortisone 109-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 10689617-7 1999 Analyses of the wild type and mutant MRs activities in response to corticosteroids bearing hydroxyl groups at various steroid skeleton position led to the following conclusions: 1) the interaction between the residue Asn 770 and the C21-hydroxyl group of corticosteroids is determinant for stabilizing the active MR conformation and 2) the stability of this conformation is enhanced by the 11-18 hemiketal group of aldosterone whereas it is decreased by the 11 beta- and 17 alpha-hydroxyl groups of cortisol. Hydrocortisone 499-507 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-39 9678540-1 1998 The mineralocorticoid receptor (MR), a member of the steroid receptor family, acts as a transcription factor and mediates both aldosterone and cortisol effects. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 9678540-1 1998 The mineralocorticoid receptor (MR), a member of the steroid receptor family, acts as a transcription factor and mediates both aldosterone and cortisol effects. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 10232052-3 1999 11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid. Hydrocortisone 265-273 nuclear receptor subfamily 3 group C member 2 Homo sapiens 78-104 9851798-1 1998 In adult life, the type 2 isozyme of 11beta-hydroxysteroid dehydrogenase (11betaHSD2) protects the mineralocorticoid receptor (MR) from glucocorticoid by inactivating cortisol to cortisone. Hydrocortisone 167-175 nuclear receptor subfamily 3 group C member 2 Homo sapiens 99-125 9851798-1 1998 In adult life, the type 2 isozyme of 11beta-hydroxysteroid dehydrogenase (11betaHSD2) protects the mineralocorticoid receptor (MR) from glucocorticoid by inactivating cortisol to cortisone. Hydrocortisone 167-175 nuclear receptor subfamily 3 group C member 2 Homo sapiens 127-129 8793850-1 1996 The 11 beta-hydroxysteroid dehydrogenase type II enzyme (11 beta HSD2) converts cortisol into mineralocorticoid receptor inactive cortisone, thus preventing occupation of the non-selective mineralocorticoid receptor by glucocorticoids in the kidney. Hydrocortisone 80-88 nuclear receptor subfamily 3 group C member 2 Homo sapiens 94-120 8793850-1 1996 The 11 beta-hydroxysteroid dehydrogenase type II enzyme (11 beta HSD2) converts cortisol into mineralocorticoid receptor inactive cortisone, thus preventing occupation of the non-selective mineralocorticoid receptor by glucocorticoids in the kidney. Hydrocortisone 80-88 nuclear receptor subfamily 3 group C member 2 Homo sapiens 189-215 8538347-1 1996 BACKGROUND: 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyses the interconversion of hormonally active cortisol to inactive cortisone and is vital for dictating specificity for the mineralocorticoid receptor. Hydrocortisone 114-122 nuclear receptor subfamily 3 group C member 2 Homo sapiens 192-218 7670488-2 1995 This enzyme normally converts cortisol to inactive cortisone and is postulated to thus confer specificity for aldosterone upon the mineralocorticoid receptor. Hydrocortisone 30-38 nuclear receptor subfamily 3 group C member 2 Homo sapiens 131-157 7575603-1 1995 The human mineralocorticoid receptor (MR) binds the agonists aldosterone and cortisol and the antagonist progesterone with a comparably high affinity. Hydrocortisone 77-85 nuclear receptor subfamily 3 group C member 2 Homo sapiens 10-36 7575603-1 1995 The human mineralocorticoid receptor (MR) binds the agonists aldosterone and cortisol and the antagonist progesterone with a comparably high affinity. Hydrocortisone 77-85 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-40 7670488-5 1995 They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension. Hydrocortisone 17-25 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-72 7545619-1 1995 11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD), responsible for the interconversion of hormonally active cortisol to inactive cortisone, dictates specificity for the mineralocorticoid receptor (MR) in the distal nephron and colon. Hydrocortisone 109-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 170-196 7545619-1 1995 11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD), responsible for the interconversion of hormonally active cortisol to inactive cortisone, dictates specificity for the mineralocorticoid receptor (MR) in the distal nephron and colon. Hydrocortisone 109-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-200 1476186-2 1992 11 beta-HSD inactivates cortisol and corticosterone, allowing the more abundantly produced glucocorticoids access to the mineralocorticoid receptor (MR) in the kidney, where they act as mineralocorticoids. Hydrocortisone 24-32 nuclear receptor subfamily 3 group C member 2 Homo sapiens 121-147 8116018-7 1993 These clinical studies, however, have uncovered a novel physiological mechanism, whereby the mineralocorticoid receptor (which in vitro has an equal affinity for cortisol and aldosterone) is protected from cortisol excess by the action of 11 beta-HSD. Hydrocortisone 162-170 nuclear receptor subfamily 3 group C member 2 Homo sapiens 93-119 8386930-8 1993 In vitro studies have shown that 11 beta-OHSD is present in aldosterone-selective tissues and acts as an autocrine mechanism which prevents cortisol from gaining access to the non-specific mineralocorticoid receptor (MR). Hydrocortisone 140-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 189-215 8386930-8 1993 In vitro studies have shown that 11 beta-OHSD is present in aldosterone-selective tissues and acts as an autocrine mechanism which prevents cortisol from gaining access to the non-specific mineralocorticoid receptor (MR). Hydrocortisone 140-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 217-219 8386930-9 1993 Congenital or acquired absence of this enzyme allows cortisol to bind to MR resulting in AME. Hydrocortisone 53-61 nuclear receptor subfamily 3 group C member 2 Homo sapiens 73-75 7792800-1 1995 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), by converting cortisol and corticosterone to hormonally inactive cortisone and 11-dehydrocorticosterone, respectively, is an important pre-receptor signaling pathway for the renal mineralocorticoid receptor (MR). Hydrocortisone 66-74 nuclear receptor subfamily 3 group C member 2 Homo sapiens 232-258 7792800-1 1995 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), by converting cortisol and corticosterone to hormonally inactive cortisone and 11-dehydrocorticosterone, respectively, is an important pre-receptor signaling pathway for the renal mineralocorticoid receptor (MR). Hydrocortisone 66-74 nuclear receptor subfamily 3 group C member 2 Homo sapiens 260-262 8319583-3 1993 One hypothesis is that 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which converts cortisol to biologically inactive cortisone, protects the mineralocorticoid receptor from cortisol. Hydrocortisone 90-98 nuclear receptor subfamily 3 group C member 2 Homo sapiens 148-174 1476186-2 1992 11 beta-HSD inactivates cortisol and corticosterone, allowing the more abundantly produced glucocorticoids access to the mineralocorticoid receptor (MR) in the kidney, where they act as mineralocorticoids. Hydrocortisone 24-32 nuclear receptor subfamily 3 group C member 2 Homo sapiens 149-151 1659446-2 1991 These contrast with the apparent in vivo selectivity of the MR in tissues such as the kidney for aldosterone in preference to cortisol despite the 100-fold molar excess of cortisol. Hydrocortisone 172-180 nuclear receptor subfamily 3 group C member 2 Homo sapiens 60-62 1659446-3 1991 This review gives the evidence that indicates that 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD), the enzyme responsible for the interconversion of cortisol and inactive cortisone, acts as a protective mechanism for the MR. Hydrocortisone 154-162 nuclear receptor subfamily 3 group C member 2 Homo sapiens 226-228 33761426-8 2021 For treatment of depression a reduction of aldosterone levels might be relevant at CNS locations specific for aldosterone, whereas MRA targets MR more broadly, including areas, where cortisol is the main ligand. Hydrocortisone 183-191 nuclear receptor subfamily 3 group C member 2 Homo sapiens 131-133 34877649-2 2021 Like in the brain, the major ligand of the MR is cortisol and the MR/glucocorticoid receptor (GR) balance regulates the activation of the MR pathway. Hydrocortisone 49-57 nuclear receptor subfamily 3 group C member 2 Homo sapiens 43-45 34316445-8 2021 The MR is unique in this family in that it binds to both aldosterone and cortisol. Hydrocortisone 73-81 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 34426510-3 2021 In this study, we show that MR is overexpressed in the retina of type 2 diabetic Goto-Kakizaki (GK) rats and humans and, that cortisol is the MR ligand in human eyes. Hydrocortisone 126-134 nuclear receptor subfamily 3 group C member 2 Homo sapiens 142-144 34579671-3 2021 Based on previous studies, it has been suggested that neurobehavioral side effects are associated to cortisol depletion of the mineralocorticoid receptor in the brain. Hydrocortisone 101-109 nuclear receptor subfamily 3 group C member 2 Homo sapiens 127-153 35579746-2 2022 The two corticoid receptors encoded by the genes NR3C1 and NR3C2 are the main players in regulating the physiological response to cortisol. Hydrocortisone 130-138 nuclear receptor subfamily 3 group C member 2 Homo sapiens 59-64 35148274-3 2022 High dosages result in strong GR activation, but likely also lower MR activation based on GR-mediated negative feedback on cortisol levels. Hydrocortisone 123-131 nuclear receptor subfamily 3 group C member 2 Homo sapiens 67-69 33249452-0 2021 New Horizons: Does Mineralocorticoid Receptor activation by cortisol cause ATP release and COVID-19 complications? Hydrocortisone 60-68 nuclear receptor subfamily 3 group C member 2 Homo sapiens 19-45 2989319-3 1985 Our data demonstrate that in normal subjects, mineralocorticoid receptor-binding steroids can be almost totally accounted for by immunoreactive deoxycorticosterone, corticosterone, cortisol, and aldo (RRA, 4.73 +/- 1.34 ng/ml aldo; RIA, 3.91 +/- 1.52 ng/ml aldo equivalents), while in 8 patients with dexamethasone-suppressible hyperaldosteronism (DSH), RRA values were greater than RIA values in the basal state (RRA, 7.57 +/- 0.75; RIA, 3.24 +/- 0.34; P less than 0.01). Hydrocortisone 181-189 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-72 3012975-12 1986 Thus, unlike Old World primates, cortisol in New World primates has only weak sodium-retaining potency because the aldosterone receptor has a low affinity for cortisol. Hydrocortisone 33-41 nuclear receptor subfamily 3 group C member 2 Homo sapiens 115-135 3012975-12 1986 Thus, unlike Old World primates, cortisol in New World primates has only weak sodium-retaining potency because the aldosterone receptor has a low affinity for cortisol. Hydrocortisone 159-167 nuclear receptor subfamily 3 group C member 2 Homo sapiens 115-135 33207294-4 2021 While the closely related glucocorticoid receptor (GR) and its ligand, cortisol (corticosterone in rodents), are established regulators of the circadian clock, new data suggest that the MR can also regulate circadian clock gene expression and timing. Hydrocortisone 71-79 nuclear receptor subfamily 3 group C member 2 Homo sapiens 186-188 33249452-2 2021 It suggests that cortisol-associated activation of the Mineralocorticoid Receptor (MR) in epithelial and endothelial cells infected with the virus stimulates the release of ATP which then acts back on purinergic receptors. Hydrocortisone 17-25 nuclear receptor subfamily 3 group C member 2 Homo sapiens 55-81 32087522-12 2020 These findings show a relationship between antenatal depression, NR3C2 DNA methylation and infant cortisol response providing support for a specific fetal programming pathway. Hydrocortisone 98-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 65-70 32467588-2 2021 The MR is a member of the nuclear receptor family of ligand-dependent transcription factors; it is unusual in being the receptor for two steroid hormones aldosterone and cortisol (which also binds to the closely related glucocorticoid receptor). Hydrocortisone 170-178 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 32499723-4 2020 One of the factors involved in stress resilience is enhanced functionality of the mineralocorticoid receptor (MR), one of the two brain receptors for the stress hormone cortisol. Hydrocortisone 169-177 nuclear receptor subfamily 3 group C member 2 Homo sapiens 82-108 32499723-4 2020 One of the factors involved in stress resilience is enhanced functionality of the mineralocorticoid receptor (MR), one of the two brain receptors for the stress hormone cortisol. Hydrocortisone 169-177 nuclear receptor subfamily 3 group C member 2 Homo sapiens 110-112 31909799-2 2020 Subtypes of essential hypertension characterized by low renin levels allowed the identification of 2 different clinical entities: aldosterone-mediated mineralocorticoid receptor (MR) activation and cortisol-mediated MR activation. Hydrocortisone 198-206 nuclear receptor subfamily 3 group C member 2 Homo sapiens 216-218 31909799-4 2020 EVIDENCE SYNTHESIS: The spectrum of cortisol-mediated MR activation includes the classic AME syndrome to milder (nonclassic) forms of AME, the latter with a much higher prevalence (7.1%) than classic AME but different phenotype and genotype. Hydrocortisone 36-44 nuclear receptor subfamily 3 group C member 2 Homo sapiens 54-56 28089704-4 2017 MR expressed in abundance in this limbic-forebrain circuitry, is target of cortisol and corticosterone in modulation of appraisal processes, memory performance and selection of coping strategy. Hydrocortisone 75-83 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2 31667853-1 2020 Severe hypercortisolism in Cushing"s syndrome may lead to a syndrome of apparent mineralocorticoid excess.1 The mineralocorticoid receptor is nonselective and has similar affinities for aldosterone and cortisol.2 In fact, the specificity of aldosterone for its renal receptor actually depends on the local inactivation of cortisol by kidney type 2 11beta-hydroxysteroid dehydrogenase,2 an enzymatic inactivation that may be overridden when very large amounts of cortisol are present. Hydrocortisone 12-20 nuclear receptor subfamily 3 group C member 2 Homo sapiens 112-138 31667853-1 2020 Severe hypercortisolism in Cushing"s syndrome may lead to a syndrome of apparent mineralocorticoid excess.1 The mineralocorticoid receptor is nonselective and has similar affinities for aldosterone and cortisol.2 In fact, the specificity of aldosterone for its renal receptor actually depends on the local inactivation of cortisol by kidney type 2 11beta-hydroxysteroid dehydrogenase,2 an enzymatic inactivation that may be overridden when very large amounts of cortisol are present. Hydrocortisone 202-210 nuclear receptor subfamily 3 group C member 2 Homo sapiens 112-138 31667853-1 2020 Severe hypercortisolism in Cushing"s syndrome may lead to a syndrome of apparent mineralocorticoid excess.1 The mineralocorticoid receptor is nonselective and has similar affinities for aldosterone and cortisol.2 In fact, the specificity of aldosterone for its renal receptor actually depends on the local inactivation of cortisol by kidney type 2 11beta-hydroxysteroid dehydrogenase,2 an enzymatic inactivation that may be overridden when very large amounts of cortisol are present. Hydrocortisone 202-210 nuclear receptor subfamily 3 group C member 2 Homo sapiens 112-138 30486399-5 2018 In terms of its signaling properties, the MR is distinct from nuclear receptors in that it has, in reality, two physiological hormonal agonists: not only aldosterone but also cortisol. Hydrocortisone 175-183 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-44 30486399-6 2018 In fact, in several tissues, including in the myocardium, cortisol is the primary hormone activating the MR. Hydrocortisone 58-66 nuclear receptor subfamily 3 group C member 2 Homo sapiens 105-107 29801983-0 2018 Corrigendum to "The role of genetic variation in the glucocorticoid receptor (NR3C1) and mineralocorticoid receptor (NR3C2) in the association between cortisol response and cognition under acute stress" [Psychoneuroendocrinology 87 (2018) 173-180]. Hydrocortisone 151-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 78-115 29801983-0 2018 Corrigendum to "The role of genetic variation in the glucocorticoid receptor (NR3C1) and mineralocorticoid receptor (NR3C2) in the association between cortisol response and cognition under acute stress" [Psychoneuroendocrinology 87 (2018) 173-180]. Hydrocortisone 151-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 117-122 31128569-0 2019 Cortisol modulates the engagement of multiple memory systems: Exploration of a common NR3C2 polymorphism. Hydrocortisone 0-8 nuclear receptor subfamily 3 group C member 2 Homo sapiens 86-91 29606180-8 2019 In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation, indirect effect = -0.07, 95% confidence interval [-0.16, -0.02]. Hydrocortisone 56-64 nuclear receptor subfamily 3 group C member 2 Homo sapiens 77-82 29100174-0 2018 The role of genetic variation in the glucocorticoid receptor (NR3C1) and mineralocorticoid receptor (NR3C2) in the association between cortisol response and cognition under acute stress. Hydrocortisone 135-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 73-99 29100174-0 2018 The role of genetic variation in the glucocorticoid receptor (NR3C1) and mineralocorticoid receptor (NR3C2) in the association between cortisol response and cognition under acute stress. Hydrocortisone 135-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 101-106 29100174-4 2018 Haplotype analyses revealed significant effects of NR3C1 (p=0.011) and NR3C2 (p=0.034) on cortisol stress response. Hydrocortisone 90-98 nuclear receptor subfamily 3 group C member 2 Homo sapiens 71-76 29100174-5 2018 NR3C2 also influenced attentional performance via an interaction with stress-induced cortisol response (p<0.001). Hydrocortisone 85-93 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-5 28938454-0 2017 11beta-HSD2 SUMOylation Modulates Cortisol-Induced Mineralocorticoid Receptor Nuclear Translocation Independently of Effects on Transactivation. Hydrocortisone 34-42 nuclear receptor subfamily 3 group C member 2 Homo sapiens 51-77 28089704-1 2017 We will highlight in honor of Randall Sakai the peculiar characteristics of the brain mineralocorticoid receptor (MR) in its response pattern to the classical mineralocorticoid aldosterone and the naturally occurring glucocorticoids corticosterone and cortisol. Hydrocortisone 252-260 nuclear receptor subfamily 3 group C member 2 Homo sapiens 86-112 28089704-1 2017 We will highlight in honor of Randall Sakai the peculiar characteristics of the brain mineralocorticoid receptor (MR) in its response pattern to the classical mineralocorticoid aldosterone and the naturally occurring glucocorticoids corticosterone and cortisol. Hydrocortisone 252-260 nuclear receptor subfamily 3 group C member 2 Homo sapiens 114-116 23025717-2 2014 We tested the hypothesis that cortisol production within the arterial wall may contribute to atherosclerotic remodeling and act through illicit activation of the mineralocorticoid receptor (MR). Hydrocortisone 30-38 nuclear receptor subfamily 3 group C member 2 Homo sapiens 162-188 27967238-0 2017 A Refill for the Brain Mineralocorticoid Receptor: The Benefit of Cortisol Add-On to Dexamethasone Therapy. Hydrocortisone 66-74 nuclear receptor subfamily 3 group C member 2 Homo sapiens 23-49 26892095-2 2017 The 11betaHSD2 enzyme confers mineralocorticoid receptor specificity for aldosterone by converting cortisol to its inactive metabolite, cortisone and inactivating the cortisol-mineralocorticoid receptor complex. Hydrocortisone 99-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 30-56 26892095-2 2017 The 11betaHSD2 enzyme confers mineralocorticoid receptor specificity for aldosterone by converting cortisol to its inactive metabolite, cortisone and inactivating the cortisol-mineralocorticoid receptor complex. Hydrocortisone 99-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 176-202 27519144-3 2016 We examined the effects of the MR antagonist spironolactone on cortisol secretion in depressed patients and healthy individuals. Hydrocortisone 63-71 nuclear receptor subfamily 3 group C member 2 Homo sapiens 31-33 27158328-2 2016 These alterations were prevented/inhibited by cortisol (Cort) or canrenone (Can) raising the hypothesis that Aldo effects in RBC may be mediated by mineralocorticoid receptor (MR), though to date MR has never been demonstrated in human RBC. Hydrocortisone 46-54 nuclear receptor subfamily 3 group C member 2 Homo sapiens 148-174 27158328-2 2016 These alterations were prevented/inhibited by cortisol (Cort) or canrenone (Can) raising the hypothesis that Aldo effects in RBC may be mediated by mineralocorticoid receptor (MR), though to date MR has never been demonstrated in human RBC. Hydrocortisone 46-54 nuclear receptor subfamily 3 group C member 2 Homo sapiens 176-178 27967238-6 2017 The refill of the unoccupied brain MR with physiological amounts of cortisol ameliorates the dexamethasone-induced psychological side effects. Hydrocortisone 68-76 nuclear receptor subfamily 3 group C member 2 Homo sapiens 35-37 25662276-1 2015 The mineralocorticoid receptor (MR) differs from the other steroid receptors in that it responds to two physiological ligands, aldosterone and cortisol. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 25662276-1 2015 The mineralocorticoid receptor (MR) differs from the other steroid receptors in that it responds to two physiological ligands, aldosterone and cortisol. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 25662276-6 2015 Molecular modelling has identified a region in the LBD of the MR and indeed other steroid receptors that critically defines ligand-specificity for aldosterone and cortisol, yet is not part of the ligand-binding pocket. Hydrocortisone 163-171 nuclear receptor subfamily 3 group C member 2 Homo sapiens 62-64 25662276-7 2015 An interaction between the N-terminus and LBD observed in the MR is aldosterone-dependent but is unexpectedly antagonised by cortisol. Hydrocortisone 125-133 nuclear receptor subfamily 3 group C member 2 Homo sapiens 62-64 24907116-1 2014 The mineralocorticoid receptor (MR) is unique in responding to 2 physiological ligands: aldosterone and cortisol. Hydrocortisone 104-112 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 24907116-1 2014 The mineralocorticoid receptor (MR) is unique in responding to 2 physiological ligands: aldosterone and cortisol. Hydrocortisone 104-112 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 24752431-11 2014 Further studies should evaluate whether mineralocorticoid receptor antagonists may reduce adverse events in individuals with chronic kidney disease because elevated cortisol levels may activate the mineralocorticoid receptor. Hydrocortisone 165-173 nuclear receptor subfamily 3 group C member 2 Homo sapiens 40-66 24752431-11 2014 Further studies should evaluate whether mineralocorticoid receptor antagonists may reduce adverse events in individuals with chronic kidney disease because elevated cortisol levels may activate the mineralocorticoid receptor. Hydrocortisone 165-173 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-224 24304824-5 2014 The present study tested the hypothesis that genetic profile scores combining variance across 10 single nucleotide polymorphisms from four stress-system genes (CRHR1, NR3C2, NR3C1, and FKBP5) and early life stress would predict increases in cortisol levels during laboratory stressors in 120 preschool-age children (3-5 years old), as well as hippocampal and amygdala volumes assessed with MRI in these same children at school age (7-12 years old). Hydrocortisone 241-249 nuclear receptor subfamily 3 group C member 2 Homo sapiens 167-172 24423282-2 2014 However, binding of aldosterone to MR requires local activity of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which inactivates cortisol to cortisone and thereby prevents receptor occupancy by cortisol. Hydrocortisone 152-160 nuclear receptor subfamily 3 group C member 2 Homo sapiens 35-37 24423282-2 2014 However, binding of aldosterone to MR requires local activity of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which inactivates cortisol to cortisone and thereby prevents receptor occupancy by cortisol. Hydrocortisone 217-225 nuclear receptor subfamily 3 group C member 2 Homo sapiens 35-37 23025717-2 2014 We tested the hypothesis that cortisol production within the arterial wall may contribute to atherosclerotic remodeling and act through illicit activation of the mineralocorticoid receptor (MR). Hydrocortisone 30-38 nuclear receptor subfamily 3 group C member 2 Homo sapiens 190-192 23025717-7 2014 MR mRNA level was lower in atheroma and lipid-storing VSMCs and downregulated via MR by fludrocortisone and cortisol. Hydrocortisone 108-116 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-2 23025717-7 2014 MR mRNA level was lower in atheroma and lipid-storing VSMCs and downregulated via MR by fludrocortisone and cortisol. Hydrocortisone 108-116 nuclear receptor subfamily 3 group C member 2 Homo sapiens 82-84 22536780-4 2012 Complexity of pathophysiological role of MR derives from the presence of circulating glucocorticoids at higher concentrations than aldosterone and the equal affinity of the MR for aldosterone, cortisol and corticosterone. Hydrocortisone 193-201 nuclear receptor subfamily 3 group C member 2 Homo sapiens 41-43 23785077-3 2013 We have shown that the MR antagonist blocked the increase in fetal heart weight and in wall thickness resulting from maternal cortisol infusion. Hydrocortisone 126-134 nuclear receptor subfamily 3 group C member 2 Homo sapiens 23-25 23446772-1 2013 Type 2 11beta-hydroxysteroid dehydrogenase encoded by the HSD11B2 gene converts cortisol to inactive cortisone and thus protects the mineralocorticoid receptor from cortisol exposure. Hydrocortisone 80-88 nuclear receptor subfamily 3 group C member 2 Homo sapiens 133-159 23446772-1 2013 Type 2 11beta-hydroxysteroid dehydrogenase encoded by the HSD11B2 gene converts cortisol to inactive cortisone and thus protects the mineralocorticoid receptor from cortisol exposure. Hydrocortisone 165-173 nuclear receptor subfamily 3 group C member 2 Homo sapiens 133-159 23443726-1 2013 BACKGROUND: Impairment in 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) activity results in inefficient inactivation of cortisol to cortisone, and it can trigger hypertension through activation of the mineralocorticoid receptor. Hydrocortisone 131-139 nuclear receptor subfamily 3 group C member 2 Homo sapiens 212-238 24133375-3 2013 Neither acts as an aldosterone antagonist in the heart as the cardiac MR are occupied by cortisol, which becomes an aldosterone mimic in conditions of tissue damage. Hydrocortisone 89-97 nuclear receptor subfamily 3 group C member 2 Homo sapiens 70-72 22536780-4 2012 Complexity of pathophysiological role of MR derives from the presence of circulating glucocorticoids at higher concentrations than aldosterone and the equal affinity of the MR for aldosterone, cortisol and corticosterone. Hydrocortisone 193-201 nuclear receptor subfamily 3 group C member 2 Homo sapiens 173-175 22723323-2 2012 Polymorphisms in the MR gene have been inconsistently shown to be associated with risk of hypertension and aldosterone and cortisol levels. Hydrocortisone 123-131 nuclear receptor subfamily 3 group C member 2 Homo sapiens 21-23 22872687-1 2012 BACKGROUND: The mineralocorticoid receptor is protected from excess of glucocorticoids by conversion of active cortisol to inactive cortisone by enzyme 11beta-hydroxysteroid dehydrogenase type 2 present in the kidney. Hydrocortisone 111-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 16-42 22872687-3 2012 HYPOTHESIS: Patients with chronic kidney disease (CKD) and essential hypertension have a functional defect in their ability to convert cortisol to cortisone, thus leading to the activation of mineralocorticoid receptor. Hydrocortisone 135-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 192-218 22723323-3 2012 The purpose of this project was to investigate the association of MR gene variants with serum aldosterone and a previously identified hypertension subgroup with higher urinary free cortisol (UFC) levels (high-mode UFC) in a rigorously phenotyped Caucasian hypertensive cohort. Hydrocortisone 181-189 nuclear receptor subfamily 3 group C member 2 Homo sapiens 66-68 22159507-1 2012 The mineralocorticoid receptor (MR) differs from the other steroid receptors in that it responds to two physiological ligands, aldosterone and cortisol. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 22159507-1 2012 The mineralocorticoid receptor (MR) differs from the other steroid receptors in that it responds to two physiological ligands, aldosterone and cortisol. Hydrocortisone 143-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 22159507-2 2012 In epithelial tissues, aldosterone selectivity is determined by the activity of 11beta-hydroxysteroid dehydrogenase type 2, while in other tissues, including the heart and regions of the central nervous system, cortisol is the primary ligand for the MR where it may act as an antagonist. Hydrocortisone 211-219 nuclear receptor subfamily 3 group C member 2 Homo sapiens 250-252 22159507-10 2012 Proteins that interact with the MR in the presence of either aldosterone or cortisol, but not both, have been identified. Hydrocortisone 76-84 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 21940729-10 2011 The beneficial effects of MR antagonism may relate to blockade of both aldosterone- and cortisol-induced MR activation. Hydrocortisone 88-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 26-28 21940729-10 2011 The beneficial effects of MR antagonism may relate to blockade of both aldosterone- and cortisol-induced MR activation. Hydrocortisone 88-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 105-107 19665310-6 2010 For this purpose we determined two single nucleotide polymorphisms (SNPs) in the MR gene, the previously described MRI180V (rs5522) and the MR-2G/C (rs2070951), which both affect in vitro the transactivational capacity of the MR in response to either cortisol or dexamethasone. Hydrocortisone 251-259 nuclear receptor subfamily 3 group C member 2 Homo sapiens 81-83 19022273-2 2009 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) is believed to confer specificity on aldosterone to activate MR by inactivating 11beta-hydroxyglucocorticoids (corticosterone, cortisol) that are 100-1000 times more abundant in plasma than aldosterone and that can also bind and activate MR. Hydrocortisone 184-192 nuclear receptor subfamily 3 group C member 2 Homo sapiens 118-120 19022273-2 2009 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) is believed to confer specificity on aldosterone to activate MR by inactivating 11beta-hydroxyglucocorticoids (corticosterone, cortisol) that are 100-1000 times more abundant in plasma than aldosterone and that can also bind and activate MR. Hydrocortisone 184-192 nuclear receptor subfamily 3 group C member 2 Homo sapiens 295-297 21164267-4 2011 The MR gene variants were associated with basal levels of cortisol, cortisol levels after dexamethasone administration and with stress-induced hypothalamic-pituitary-adrenal axis and autonomic reactivity. Hydrocortisone 58-66 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 20528958-2 2010 The mineralocorticoid receptor (MR) determines the sensitivity of the stress response, and the missense iso/val polymorphism (Ile180Val, rs5522) of the MR gene (NR3C2) has been associated with enhanced physiological stress responses, elevated depressive symptoms and reduced cortisol-induced MR gene expression. Hydrocortisone 275-283 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 20528958-2 2010 The mineralocorticoid receptor (MR) determines the sensitivity of the stress response, and the missense iso/val polymorphism (Ile180Val, rs5522) of the MR gene (NR3C2) has been associated with enhanced physiological stress responses, elevated depressive symptoms and reduced cortisol-induced MR gene expression. Hydrocortisone 275-283 nuclear receptor subfamily 3 group C member 2 Homo sapiens 152-154 20528958-2 2010 The mineralocorticoid receptor (MR) determines the sensitivity of the stress response, and the missense iso/val polymorphism (Ile180Val, rs5522) of the MR gene (NR3C2) has been associated with enhanced physiological stress responses, elevated depressive symptoms and reduced cortisol-induced MR gene expression. Hydrocortisone 275-283 nuclear receptor subfamily 3 group C member 2 Homo sapiens 161-166 20528958-2 2010 The mineralocorticoid receptor (MR) determines the sensitivity of the stress response, and the missense iso/val polymorphism (Ile180Val, rs5522) of the MR gene (NR3C2) has been associated with enhanced physiological stress responses, elevated depressive symptoms and reduced cortisol-induced MR gene expression. Hydrocortisone 275-283 nuclear receptor subfamily 3 group C member 2 Homo sapiens 152-154 19648477-1 2010 The mineralocorticoid receptor (MR) has been called a promiscuous receptor because its intrinsic affinity for aldosterone, cortisol and corticosterone is similar. Hydrocortisone 123-131 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 19648477-1 2010 The mineralocorticoid receptor (MR) has been called a promiscuous receptor because its intrinsic affinity for aldosterone, cortisol and corticosterone is similar. Hydrocortisone 123-131 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 19641483-2 2009 Because glycyrrhetinic acid (GA) inhibits the enzyme 11beta-hydroxy-steroid dehydrogenase II and thereby increases cortisol availability to the colonic mineralocorticoid receptor, it has the potential to lower serum potassium concentrations. Hydrocortisone 115-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 152-178 19541744-4 2009 By using a range of natural and synthetic MR ligands in a mammalian two-hybrid assay we demonstrate that in contrast to aldosterone, which strongly induces the interaction, the physiological ligands deoxycorticosterone and cortisol weakly promote the interaction but predominantly inhibit the aldosterone-mediated N/C-interaction. Hydrocortisone 223-231 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-44