PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7626473-2 1995 Due to the difference in affinity of the two receptor types for corticosterone and variations in endogenous steroid levels, occupation of the receptors will range between a situation of predominant mineralocorticoid receptor activation and conditions where both receptor types are occupied. Steroids 108-115 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-224 8612804-5 1996 Steroid modulation of the interaction between domain E and actin indicated that this actin binding is specific and could be essential for cellular mineralocorticoid receptor activity. Steroids 0-7 nuclear receptor subfamily 3 group C member 2 Homo sapiens 147-173 8645616-0 1996 Putative steroid binding domain of the human mineralocorticoid receptor, expressed in E. coli in the presence of heat shock proteins shows typical native receptor characteristics. Steroids 9-16 nuclear receptor subfamily 3 group C member 2 Homo sapiens 45-71 8732998-5 1996 The discovery of abnormal binding of aldosterone to the mineralocorticoid receptor (MR) in lymphocytes from affected patients, by analogy to findings in other syndromes of steroid hormone resistance, led to the hypothesis that the disease reflected a molecular defect in MR, which has prompted a series of molecular studies to characterize the defect. Steroids 172-187 nuclear receptor subfamily 3 group C member 2 Homo sapiens 56-82 7804754-4 1994 The discovery of variable activity of several steroids on the mineralocorticoid receptor has provided additional understanding of the finding of the manifestations of hyperaldosteronism in the presence of normal aldosterone production. Steroids 46-54 nuclear receptor subfamily 3 group C member 2 Homo sapiens 62-88 8185571-2 1994 Binding of RU 26752, a ligand specific to the MCR, suggests 100 fmol steroid bound per mg of tobacco protein; this is equivalent to about 6000 sites per cell assuming a 1/1 stoichiometry. Steroids 69-76 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-49 8388719-6 1993 On the other hand, in vitro incubation of monomeric GR or MR partially purified from the insoluble receptor aggregates with reticulocyte lysate resulted in complete reconstitution of the oligomeric receptor complex with a concomitant restoration of full steroid binding ability. Steroids 254-261 nuclear receptor subfamily 3 group C member 2 Homo sapiens 58-60 8282004-2 1993 The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. Steroids 8-15 nuclear receptor subfamily 3 group C member 2 Homo sapiens 120-146 8282004-2 1993 The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. Steroids 8-15 nuclear receptor subfamily 3 group C member 2 Homo sapiens 215-241 34740745-0 2022 Non-genomic steroid signaling through the mineralocorticoid receptor: Involvement of a membrane-associated receptor? Steroids 12-19 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-68 1734933-1 1992 11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD) dictates specificity for the mineralocorticoid receptor (MR) by converting the active steroid cortisol to cortisone in man (corticosterone to 11-dehydrocorticosterone in rodents), leaving aldosterone to occupy the MR. Steroids 15-22 nuclear receptor subfamily 3 group C member 2 Homo sapiens 80-106 1734933-1 1992 11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD) dictates specificity for the mineralocorticoid receptor (MR) by converting the active steroid cortisol to cortisone in man (corticosterone to 11-dehydrocorticosterone in rodents), leaving aldosterone to occupy the MR. Steroids 15-22 nuclear receptor subfamily 3 group C member 2 Homo sapiens 108-110 34316445-1 2021 The glucocorticoid receptor (GCR) and the mineralocorticoid receptor (MR) are members of the steroid receptor superfamily of hormone-dependent transcription factors. Steroids 93-100 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-68 34811739-1 2021 During the past decades, the mineralocorticoid receptor (MR) has evolved from a much-overlooked member of the steroid hormone receptor family to an important player, not only in volume and electrolyte homeostasis, but also in pathological changes occurring in an increasing number of tissues, especially the renal and cardiovascular systems. Steroids 110-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 29-55 34811739-1 2021 During the past decades, the mineralocorticoid receptor (MR) has evolved from a much-overlooked member of the steroid hormone receptor family to an important player, not only in volume and electrolyte homeostasis, but also in pathological changes occurring in an increasing number of tissues, especially the renal and cardiovascular systems. Steroids 110-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 57-59 34228431-1 2021 The mineralocorticoid receptor (MR) is a nuclear receptor whose endogenous ligands are mineralocorticoids, a type of steroid hormone. Steroids 117-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 34316445-1 2021 The glucocorticoid receptor (GCR) and the mineralocorticoid receptor (MR) are members of the steroid receptor superfamily of hormone-dependent transcription factors. Steroids 93-100 nuclear receptor subfamily 3 group C member 2 Homo sapiens 70-72 2856104-3 1988 This identification is supported by the anatomical distribution of MR mRNA, determined by in situ hybridization histochemistry, which parallels the steroid autoradiographic localization of the type I sites. Steroids 148-155 nuclear receptor subfamily 3 group C member 2 Homo sapiens 67-69 35149051-3 2022 Here I discuss that due to evolution of the progesterone receptor (PR) and mineralocorticoid receptor (MR) after ray-finned fish and terrestrial vertebrates diverged from a common ancestor, each receptor evolved to respond to different steroids in ray-finned fish and terrestrial vertebrates. Steroids 236-244 nuclear receptor subfamily 3 group C member 2 Homo sapiens 75-101 35149051-3 2022 Here I discuss that due to evolution of the progesterone receptor (PR) and mineralocorticoid receptor (MR) after ray-finned fish and terrestrial vertebrates diverged from a common ancestor, each receptor evolved to respond to different steroids in ray-finned fish and terrestrial vertebrates. Steroids 236-244 nuclear receptor subfamily 3 group C member 2 Homo sapiens 103-105 3040999-3 1987 Several steroid derivatives having the delta 11-pregnane skeleton with a 17-gamma-spirolactone function were synthesized to evaluate their antialdosterone activity and to elucidate the relation between their binding affinity to mineralocorticoid receptor (MR) and their mineralo- and/or antimineralocorticoid activity. Steroids 8-15 nuclear receptor subfamily 3 group C member 2 Homo sapiens 228-254 3040999-3 1987 Several steroid derivatives having the delta 11-pregnane skeleton with a 17-gamma-spirolactone function were synthesized to evaluate their antialdosterone activity and to elucidate the relation between their binding affinity to mineralocorticoid receptor (MR) and their mineralo- and/or antimineralocorticoid activity. Steroids 8-15 nuclear receptor subfamily 3 group C member 2 Homo sapiens 256-258 1071637-14 1976 However, an increase in plasma steroids which bind to the mineralocorticoid receptor was not detected in plasma from patients with "low-renin essential hypertension". Steroids 31-39 nuclear receptor subfamily 3 group C member 2 Homo sapiens 58-84 3007560-2 1986 In normal subjects and patients with other disorders, the mineralocorticoid receptor-binding activity in such extracts could be entirely accounted for by the sum of the contributions of the steroids known to bind to the mineralocorticoid receptor. Steroids 190-198 nuclear receptor subfamily 3 group C member 2 Homo sapiens 58-84 3007560-2 1986 In normal subjects and patients with other disorders, the mineralocorticoid receptor-binding activity in such extracts could be entirely accounted for by the sum of the contributions of the steroids known to bind to the mineralocorticoid receptor. Steroids 190-198 nuclear receptor subfamily 3 group C member 2 Homo sapiens 220-246 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). Steroids 81-89 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-72 33713045-1 2021 In vertebrates, the mineralocorticoid receptor (MR) is a steroid-activated nuclear receptor (NR) that plays essential roles in water-electrolyte balance and blood pressure homeostasis. Steroids 57-64 nuclear receptor subfamily 3 group C member 2 Homo sapiens 20-46 33713045-1 2021 In vertebrates, the mineralocorticoid receptor (MR) is a steroid-activated nuclear receptor (NR) that plays essential roles in water-electrolyte balance and blood pressure homeostasis. Steroids 57-64 nuclear receptor subfamily 3 group C member 2 Homo sapiens 48-50 32800933-5 2020 Importantly, we found increased mRNA expression of genes coding for the cytokines (il15 and il34), steroid receptors (nr3c2) and oxidative stress marker enzymes (gpx1 and sod1) in the spleen, suggesting the activation of both immune and antioxidant molecular pathways during the early photostimulated state. Steroids 99-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 118-123 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). Steroids 137-144 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-6 32064789-4 2020 Interestingly, the NR3C2 gene encodes the MR protein, a steroid hormone-regulated transcription factor that acts in the hypothalamic-pituitary-adrenal axis and has been connected to stress and anxiety, both of which are features often seen in individuals with autism. Steroids 56-63 nuclear receptor subfamily 3 group C member 2 Homo sapiens 19-24 32739288-4 2020 P4 and the synthetic progestins have a hugely variable affinity for binding not only to the P4 receptors but also to other members of the steroid receptor family including glucocorticoid receptor, androgen receptor and mineralocorticoid receptor. Steroids 138-145 nuclear receptor subfamily 3 group C member 2 Homo sapiens 219-245 32064789-4 2020 Interestingly, the NR3C2 gene encodes the MR protein, a steroid hormone-regulated transcription factor that acts in the hypothalamic-pituitary-adrenal axis and has been connected to stress and anxiety, both of which are features often seen in individuals with autism. Steroids 56-63 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-44 31821037-7 2020 Luciferase reporter gene assays were performed on transfected HEK293T cells while in silico modelling examined structural interactions between these steroids within ligand-binding domain of MR. Steroids 149-157 nuclear receptor subfamily 3 group C member 2 Homo sapiens 190-192 28956026-9 2016 Moreover, combining the MR antagonist with clinically used steroids is more effective in reducing pain behaviors than using the steroids alone. Steroids 128-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 24-26 30678853-7 2019 Since there are now recognized gender differences in cardiovascular disease, we also include preliminary studies to investigate the interaction of sex steroid hormones with the ligand binding pocket of the mineralocorticoid receptor. Steroids 151-167 nuclear receptor subfamily 3 group C member 2 Homo sapiens 206-232 30532752-5 2018 Cell-specific steroid signaling was determined by mRNA expression of pre-receptor regulation (11beta-hydroxysteroid dehydrogenase type 1; 11beta -HSD1), steroid receptor expression [glucocorticoid receptor (GR) and mineralocorticoid receptor (MR)], and the downstream target glucocorticoid-induced leucine-zipper (GILZ). Steroids 14-21 nuclear receptor subfamily 3 group C member 2 Homo sapiens 215-241 30532752-5 2018 Cell-specific steroid signaling was determined by mRNA expression of pre-receptor regulation (11beta-hydroxysteroid dehydrogenase type 1; 11beta -HSD1), steroid receptor expression [glucocorticoid receptor (GR) and mineralocorticoid receptor (MR)], and the downstream target glucocorticoid-induced leucine-zipper (GILZ). Steroids 14-21 nuclear receptor subfamily 3 group C member 2 Homo sapiens 243-245 30140452-0 2018 Mineralocorticoid Receptor Antagonist Treatment for Steroid-Induced Central Serous Chorioretinopathy Patients with Continuous Systemic Steroid Treatment. Steroids 52-59 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 30140452-0 2018 Mineralocorticoid Receptor Antagonist Treatment for Steroid-Induced Central Serous Chorioretinopathy Patients with Continuous Systemic Steroid Treatment. Steroids 135-142 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 30140452-1 2018 Purpose: To investigate the effectiveness of mineralocorticoid receptor (MR) antagonist in patients with steroid-induced central serous chorioretinopathy (CSC). Steroids 105-112 nuclear receptor subfamily 3 group C member 2 Homo sapiens 45-71 30140452-1 2018 Purpose: To investigate the effectiveness of mineralocorticoid receptor (MR) antagonist in patients with steroid-induced central serous chorioretinopathy (CSC). Steroids 105-112 nuclear receptor subfamily 3 group C member 2 Homo sapiens 73-75 30140452-2 2018 Methods: A retrospective review was conducted of steroid-induced CSC patients who were treated with the MR antagonist spironolactone 50 mg once per day for at least 1 month. Steroids 49-56 nuclear receptor subfamily 3 group C member 2 Homo sapiens 104-106 30140452-12 2018 Conclusion: MR antagonist treatment may be a therapeutic option for steroid-induced CSC patients. Steroids 68-75 nuclear receptor subfamily 3 group C member 2 Homo sapiens 12-14 29668907-1 2018 The mineralocorticoid receptor (MR) is a member of the nuclear receptor steroid-binding family. Steroids 72-79 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 29668907-1 2018 The mineralocorticoid receptor (MR) is a member of the nuclear receptor steroid-binding family. Steroids 72-79 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 28634268-2 2017 At that time, spirolactone, the first generation of synthetic steroid-based MR antagonists (MRAs), which was identified in preclinical in vivo models, had already been in clinical use for 30 years. Steroids 62-69 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-78 26634965-2 2016 While traditional steroid-based MR antagonists effectively reduce mortality rates and extend patient survival, their broad application has been limited by significant side effects, most notably hyperkalaemia. Steroids 18-25 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 28956026-0 2016 Mineralocorticoid Receptor, A Promising Target for Improving Management of Low Back Pain by Epidural Steroid Injections. Steroids 101-108 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 28956026-2 2016 In this review, we aim to show that mineralocorticoid receptor (MR) activation has a critical role in the initiation of immune and inflammatory responses, which in turn can impact the effectiveness of the currently used steroids for epidural injections in low back pain management since most steroids activate MR in addition to the primary target, glucocorticoid receptor (GR). Steroids 220-228 nuclear receptor subfamily 3 group C member 2 Homo sapiens 36-62 28956026-2 2016 In this review, we aim to show that mineralocorticoid receptor (MR) activation has a critical role in the initiation of immune and inflammatory responses, which in turn can impact the effectiveness of the currently used steroids for epidural injections in low back pain management since most steroids activate MR in addition to the primary target, glucocorticoid receptor (GR). Steroids 220-228 nuclear receptor subfamily 3 group C member 2 Homo sapiens 64-66 28956026-2 2016 In this review, we aim to show that mineralocorticoid receptor (MR) activation has a critical role in the initiation of immune and inflammatory responses, which in turn can impact the effectiveness of the currently used steroids for epidural injections in low back pain management since most steroids activate MR in addition to the primary target, glucocorticoid receptor (GR). Steroids 220-228 nuclear receptor subfamily 3 group C member 2 Homo sapiens 310-312 28956026-2 2016 In this review, we aim to show that mineralocorticoid receptor (MR) activation has a critical role in the initiation of immune and inflammatory responses, which in turn can impact the effectiveness of the currently used steroids for epidural injections in low back pain management since most steroids activate MR in addition to the primary target, glucocorticoid receptor (GR). Steroids 292-300 nuclear receptor subfamily 3 group C member 2 Homo sapiens 36-62 28956026-2 2016 In this review, we aim to show that mineralocorticoid receptor (MR) activation has a critical role in the initiation of immune and inflammatory responses, which in turn can impact the effectiveness of the currently used steroids for epidural injections in low back pain management since most steroids activate MR in addition to the primary target, glucocorticoid receptor (GR). Steroids 292-300 nuclear receptor subfamily 3 group C member 2 Homo sapiens 64-66 28956026-10 2016 SUMMARY: MR antagonists are promising candidates to increase the effectiveness of currently used steroids. Steroids 97-105 nuclear receptor subfamily 3 group C member 2 Homo sapiens 9-11 22455832-8 2012 In addition, steroid sensitivity of T cell proliferation was tested using hydrocortisone as well as MR (aldosterone) and GR (dexamethasone) agonists. Steroids 13-20 nuclear receptor subfamily 3 group C member 2 Homo sapiens 100-102 25251318-2 2015 Cardiomyocytes are mostly devoid of nuclear glucocorticoid receptors (GRs) and it is generally assumed that effects of adrenal steroids in heart are mediated through the mineralocorticoid receptor (MR). Steroids 127-135 nuclear receptor subfamily 3 group C member 2 Homo sapiens 170-196 25251318-2 2015 Cardiomyocytes are mostly devoid of nuclear glucocorticoid receptors (GRs) and it is generally assumed that effects of adrenal steroids in heart are mediated through the mineralocorticoid receptor (MR). Steroids 127-135 nuclear receptor subfamily 3 group C member 2 Homo sapiens 198-200 25896481-0 2015 Influence of 17-Hydroxyprogesterone, Progesterone and Sex Steroids on Mineralocorticoid Receptor Transactivation in Congenital Adrenal Hyperplasia. Steroids 58-66 nuclear receptor subfamily 3 group C member 2 Homo sapiens 70-96 25896481-3 2015 Therefore, we analysed the effect of accumulated steroids [17-hydroxyprogesterone (17OHP), progesterone, androstenedione and testosterone] on aldosterone-mediated transactivation of the human mineralocorticoid receptor (hMR). Steroids 49-57 nuclear receptor subfamily 3 group C member 2 Homo sapiens 192-218 17647025-6 2009 In another group, abnormal adrenal steroid production leads to inappropriate stimulation of the mineralocorticoid receptor (MR) in the distal nephron. Steroids 35-42 nuclear receptor subfamily 3 group C member 2 Homo sapiens 96-122 17647025-6 2009 In another group, abnormal adrenal steroid production leads to inappropriate stimulation of the mineralocorticoid receptor (MR) in the distal nephron. Steroids 35-42 nuclear receptor subfamily 3 group C member 2 Homo sapiens 124-126 19523507-0 2009 Mixed-model QSAR at the human mineralocorticoid receptor: predicting binding mode and affinity of anabolic steroids. Steroids 107-115 nuclear receptor subfamily 3 group C member 2 Homo sapiens 30-56 19549592-1 2009 Aldosterone, the endogenous ligand of the mineralocorticoid receptor (MR) in humans, is a steroid hormone that regulates salt and water homeostasis. Steroids 90-105 nuclear receptor subfamily 3 group C member 2 Homo sapiens 42-68 19549592-1 2009 Aldosterone, the endogenous ligand of the mineralocorticoid receptor (MR) in humans, is a steroid hormone that regulates salt and water homeostasis. Steroids 90-105 nuclear receptor subfamily 3 group C member 2 Homo sapiens 70-72 17105867-2 2007 Many natural and synthetic steroids can also bind to the MR to produce agonist or antagonist effects. Steroids 27-35 nuclear receptor subfamily 3 group C member 2 Homo sapiens 57-59 18284228-0 2008 A DFT-D investigation of the mechanisms for activation of the wild-type and S810L mutated mineralocorticoid receptor by steroid hormones. Steroids 120-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 90-116 18001136-9 2007 Each hormone/MR complex yielded different proteolytic peptide patterns, suggesting that MR acquires different conformations upon steroid binding. Steroids 129-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 13-15 18001136-9 2007 Each hormone/MR complex yielded different proteolytic peptide patterns, suggesting that MR acquires different conformations upon steroid binding. Steroids 129-136 nuclear receptor subfamily 3 group C member 2 Homo sapiens 88-90 17105867-9 2007 Docking of steroids within the crystal structure of the ligand-binding domain of MR, together with trans-activation studies, revealed that the contacts between the 17beta-hydroxyl group of androgens and the Asn770, Cys942, and Thr945 residues of the ligand-binding cavity stabilize ligand binding complexes but are not strong enough to keep the receptor in its active state. Steroids 11-19 nuclear receptor subfamily 3 group C member 2 Homo sapiens 81-83 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. Steroids 126-134 nuclear receptor subfamily 3 group C member 2 Homo sapiens 90-116 16837642-11 2006 These data indicate that macaque granulosa cells can synthesize mineralocorticoids in response to an ovulatory stimulus and that the mineralocorticoid receptor plays a key role in steroid synthesis associated with luteinization of macaque granulosa cells. Steroids 180-187 nuclear receptor subfamily 3 group C member 2 Homo sapiens 133-159 15993578-8 2005 Since MR is a known mineralocorticoid-responsive gene as well as an intracellular receptor molecule for this steroid, these results suggest that locally produced aldosterone is biologically active, stimulating the transcription rates of the mineralocorticoid-responsive genes by activating the MR in mesangial cells. Steroids 109-116 nuclear receptor subfamily 3 group C member 2 Homo sapiens 6-8 15737989-2 2005 Steroid treatment transforms MR from a transcriptionally inert state, in which it is distributed equally between the nucleus and cytoplasm, to an active completely nuclear transcription factor. Steroids 0-7 nuclear receptor subfamily 3 group C member 2 Homo sapiens 29-31 15737989-10 2005 NL1 acted in concert with NL0 and NL2 to stimulate nuclear uptake of the agonist-treated receptor, but also directed the complete nuclear localization of MR in response to treatment with steroid antagonist. Steroids 187-194 nuclear receptor subfamily 3 group C member 2 Homo sapiens 154-156 12538613-2 2003 All steroids, including progesterone, that display antagonist properties when bound to the wild-type MR are able to activate the mutant receptor (MR(L810)). Steroids 4-12 nuclear receptor subfamily 3 group C member 2 Homo sapiens 101-103 12538613-2 2003 All steroids, including progesterone, that display antagonist properties when bound to the wild-type MR are able to activate the mutant receptor (MR(L810)). Steroids 4-12 nuclear receptor subfamily 3 group C member 2 Homo sapiens 146-148 12538613-4 2003 However, the steroid(s) responsible for hypertension in MR(L810) carriers (men and nonpregnant women) has not yet been identified. Steroids 13-20 nuclear receptor subfamily 3 group C member 2 Homo sapiens 56-58 16256010-3 2005 Other steroid hormones that are aldosterone and cortisol precursors also activate the mineralocorticoid receptor and cause hypertension when overproduced. Steroids 6-13 nuclear receptor subfamily 3 group C member 2 Homo sapiens 86-112 15761029-6 2005 On the other hand, we have identified coactivator binding groove mutations that are critical for cortisol activation but not for aldosterone activation, suggesting that the two steroids induce different MR LBD conformations. Steroids 177-185 nuclear receptor subfamily 3 group C member 2 Homo sapiens 203-205 15134815-2 2004 The first step in the genomic-dependent mechanism of action of mineralocorticoids is the binding of steroid to the MR, which in turn triggers MR nuclear translocation. Steroids 100-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 115-117 15134815-2 2004 The first step in the genomic-dependent mechanism of action of mineralocorticoids is the binding of steroid to the MR, which in turn triggers MR nuclear translocation. Steroids 100-107 nuclear receptor subfamily 3 group C member 2 Homo sapiens 142-144 15134815-3 2004 The regulation of hormone-binding to MR is complex and involves a multifactorial mechanism, making it difficult to determine the optimal structure of a steroid for activating the MR and promoting its nuclear translocation. Steroids 152-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-39 15134815-3 2004 The regulation of hormone-binding to MR is complex and involves a multifactorial mechanism, making it difficult to determine the optimal structure of a steroid for activating the MR and promoting its nuclear translocation. Steroids 152-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 179-181 15134816-0 2004 Identification of steroid ligands able to inactivate the mineralocorticoid receptor harboring the S810L mutation responsible for a severe form of hypertension. Steroids 18-25 nuclear receptor subfamily 3 group C member 2 Homo sapiens 57-83 15134816-1 2004 The ability of steroid ligands to inactivate the human mineralocorticoid receptor (MR(WT)) has been shown to be due to their inability to contact Asn770, a residue of the H3 helix involved in stabilizing contacts with the H11-H12 loop region. Steroids 15-22 nuclear receptor subfamily 3 group C member 2 Homo sapiens 55-81 12933324-1 2003 The authors studied mineralocorticoid receptor (MCR)-mediated effects of steroids on CD34(+) progenitor cells. Steroids 73-81 nuclear receptor subfamily 3 group C member 2 Homo sapiens 20-46 12933324-1 2003 The authors studied mineralocorticoid receptor (MCR)-mediated effects of steroids on CD34(+) progenitor cells. Steroids 73-81 nuclear receptor subfamily 3 group C member 2 Homo sapiens 48-51 10860927-1 2000 We have demonstrated previously that a planar conformation of the molecular frame is required for steroids to acquire optimal sodium-retaining activity and binding properties to the mineralocorticoid receptor (MR). Steroids 98-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 182-208 11909639-1 2002 The alkylation of amino groups of the mineralocorticoid receptor (MR) with pyridoxal 5"-phosphate or 2,4,6-trinitrobenzenesulphonate (TNBS) under controlled conditions modifies only one lysyl residue, which accounts for a 70% inhibition of steroid binding capacity. Steroids 240-247 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-64 11909639-1 2002 The alkylation of amino groups of the mineralocorticoid receptor (MR) with pyridoxal 5"-phosphate or 2,4,6-trinitrobenzenesulphonate (TNBS) under controlled conditions modifies only one lysyl residue, which accounts for a 70% inhibition of steroid binding capacity. Steroids 240-247 nuclear receptor subfamily 3 group C member 2 Homo sapiens 66-68 10884226-3 2000 This mutation results in constitutive MR activity and alters receptor specificity, with progesterone and other steroids lacking 21-hydroxyl groups, normally MR antagonists, becoming potent agonists. Steroids 111-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-40 11740142-12 2001 (c) The activating mutation of the MR results in constitutive MR activity and alters receptor specificity, with progesterone and other steroids lacking 21-hydroxyl groups becoming potent agonists. Steroids 135-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 35-37 11740142-12 2001 (c) The activating mutation of the MR results in constitutive MR activity and alters receptor specificity, with progesterone and other steroids lacking 21-hydroxyl groups becoming potent agonists. Steroids 135-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 62-64 10860927-8 2000 In addition, the binding properties of both steroids are differentially affected by modification of crucial lysyl residues of the MR. Steroids 44-52 nuclear receptor subfamily 3 group C member 2 Homo sapiens 130-132 10860927-1 2000 We have demonstrated previously that a planar conformation of the molecular frame is required for steroids to acquire optimal sodium-retaining activity and binding properties to the mineralocorticoid receptor (MR). Steroids 98-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 210-212 10329476-1 1999 The mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) belong to the steroid/thyroid hormone superfamily of ligand-induced transcription factors. Steroids 83-90 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 10329476-1 1999 The mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) belong to the steroid/thyroid hormone superfamily of ligand-induced transcription factors. Steroids 83-90 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 9724527-0 1998 Cysteines 849 and 942 of human mineralocorticoid receptor are crucial for steroid binding. Steroids 74-81 nuclear receptor subfamily 3 group C member 2 Homo sapiens 31-57 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. Steroids 74-81 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-39 9774704-0 1998 Photoaffinity labelling of the human mineralocorticoid receptor with steroids having a reactive group at position 3, 18 or 21. Steroids 69-77 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-63 9344633-5 1997 The isolated mineralocorticoid receptor binds several adrenal steroids, including aldosterone and the major glucocorticoids, with equal affinity. Steroids 62-70 nuclear receptor subfamily 3 group C member 2 Homo sapiens 13-39 9392437-1 1997 The human mineralocorticoid receptor (MR) is a member of the steroid-thyroid hormone receptor superfamily, which includes receptors for retinoic acid, vitamin D, and other steroids, such as the glucocorticoids (which bind the glucocorticoid receptor, GR). Steroids 172-180 nuclear receptor subfamily 3 group C member 2 Homo sapiens 10-36 9392437-1 1997 The human mineralocorticoid receptor (MR) is a member of the steroid-thyroid hormone receptor superfamily, which includes receptors for retinoic acid, vitamin D, and other steroids, such as the glucocorticoids (which bind the glucocorticoid receptor, GR). Steroids 172-180 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-40