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anti-Human NR3C2 Antikörper:
anti-Rat (Rattus) NR3C2 Antikörper:
anti-Mouse (Murine) NR3C2 Antikörper:
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Human Polyclonal NR3C2 Primary Antibody für IF (p), IHC (p) - ABIN735353
Liu, Jiang, Zhang, Li, Li, Xie, Hu: Pulmonary artery denervation improves pulmonary arterial hypertension induced right ventricular dysfunction by modulating the local renin-angiotensin-aldosterone system. in BMC cardiovascular disorders 2016
Chicken Monoclonal NR3C2 Primary Antibody für BP, FACS - ABIN152721
Leite-Dellova, Szriber, Merighe, Polidoro, Rebouças, Oliveira-Souza, de Mello-Aires: Signaling pathways involved in the rapid biphasic effect of aldosterone on Na+/H+ exchanger in rat proximal tubule cells. in The Journal of steroid biochemistry and molecular biology 2018
Human Polyclonal NR3C2 Primary Antibody für WB - ABIN3043575
Rigiracciolo, Scarpelli, Lappano, Pisano, Santolla, Avino, De Marco, Bussolati, Maggiolini, De Francesco: GPER is involved in the stimulatory effects of aldosterone in breast cancer cells and breast tumor-derived endothelial cells. in Oncotarget 2016
Human Polyclonal NR3C2 Primary Antibody für IHC, IHC (p) - ABIN4334537
Ong, Chng, Meaney, Buschdorf: Decreased hippocampal mineralocorticoid:glucocorticoid receptor ratio is associated with low birth weight in female cynomolgus macaque neonates. in Journal of molecular endocrinology 2013
Data demonstrate that there are distinct differences between the human mineralocorticoid receptor (MR) and the zebrafish MR despite considerable sequence and functional conservation.
HuR-dependent editing of a new mineralocorticoid receptor splice variant reveals an osmoregulatory loop for sodium homeostasis.
Role of mineralocorticoid receptor activation in cardiac diastolic dysfunction.
MiR-135b-5p, maybe a novel therapeutic target for pancreatic cancer, promoted migration, invasion and EMT of pancreatic cancer cells by targeting NR3C2.
Our findings indicate that genetic variants associated with enhanced mineralocorticoid receptor expression facilitate a stress-induced shift from hippocampal toward dorsal striatal learning, most likely via impaired hippocampal processing and reduced amygdala-hippocampus cross talk, allowing the dorsal striatum to guide behavior under stress.
We genotyped 4 SNPs on the NR3C2 gene (rs6810951, rs4635799, rs11099695, rs2070950. Haplotype analyses revealed significant effects of NR3C2 (p = 0.034) on cortisol stress response.NR3C2 also influenced attentional performance via an interaction with stress-induced cortisol response (p < 0.001). Neither NR3C1 haplotype nor NR3C2 haplotype was associated with reasoning abilities.
Corticosterone coordinates via mineralocorticoid receptor the networks underlying how an individual copes with stress, and this action is complemented by the widely distributed lower affinity glucocorticoid receptor involved in the subsequent management of stress adaptation.
The MR-genotype moderates the influence of E2 and P4 on emotional information processing.
SUMOylation of 11beta-HSD2 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) 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 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 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) and Mineralocorticoid Receptor (MR) actions on NFkappaB - and AP-1-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-driven transcription in these cells.
The inhibitory effect of phosphorylation on MR acts in a dominant-negative manner, effectively amplifying its functional effect on gene transactivation.
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, and PTGES3 in autistic spectrum disorder (ASD) and suggest a possible role of inflammation in altered GR function in ASD.
hyperactive hypothalamo-pituitary-adrenocortical axis in overweight diabetic subjects may be associated with downregulation of 11beta-HSD1, MR, and GR in the brain.
MR C3514G and MR C4582A single nucleotide polymorphism exhibited no association with the development of coronary artery disease in Taiwanese.
Our current findings demonstrate that Arctigenin is an antagonist of MR and effectively decreases the Na/K-ATPase 1 gene expression. Our work provides a hint for the drug discovery against cardiovascular disease
Data show that both mineralcorticoid receptor (MR) and G-protein estrogen receptor (GPER) contribute to the proliferation and migration of breast and endothelial cancer cells by sodium-hydrogen exchanger 1 protein (NHE-1) upon aldosterone exposure.
Endothelial mineralocorticoid receptor contributes to the transition of cardiac hypertrophy to systolic dysfunction.
These findings describe an original mechanism involving a phosphatase in the regulation of aldosterone signaling and provide new and important insights into the molecular mechanism underlying the MR turnover.
myeloid MR knockout (MRKO) improves glucose intolerance, insulin 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.
MR deficiency suppresses macrophage foam cell formation and up-regulates expression of genes related to cholesterol efflux, as well as increases effective efferocytosis and phagocytic capacity of macrophages.
Nr3c2 has a role in mouse skin development in a process that involves HSD11B1/HSD11B2
MR function is important in the stress response in the mouse hippocampus.
Inducible Knock-Down of the Mineralocorticoid Receptor in Mice Disturbs Regulation of the Renin-Angiotensin-Aldosterone System and Attenuates Heart Failure Induced by Pressure Overload
overexpression of MRs may confer resilience to the effects of chronic stress on hippocampus-dependent function and structural plasticity.
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.
Endothelial mineralocorticoid receptors participate in regulation of vasomotor function in a vascular bed-specific manner that is also modulated by risk factors, such as hypertension.
mRNA expression of MR is decreased in the amygdala of serotonin deficient mice after early life stress.
a cooperative role of MR and cav-1 in regulating vascular contraction and NO-cGMP-mediated relaxation during low NO-high AngII-dependent cardiovascular injury
The MR C603S mutant mice either die at birth or fail to thrive, lose weight, and die between days 10 and 13 in a manner similar to that observed previously for mice null for the MR gene. The nice could be rescued by twice-daily saline injections.
Upregulation of MR in mouse adipocytes led to increased weight and fat mass, insulin 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 increased in pressure-overload-mice.
Data indicated that MR deficiency in myeloid cells effectively attenuated aortic constriction-induced cardiac hypertrophy and fibrosis, as well as aortic fibrosis and inflammation.
Aldosterone may mediate the pathogenic actions of MR in the retina. A functional retinal MR-aldosterone system was seen with MR expression & translocation of nuclear MR. MR and aldosterone influence retinal vasculopathy.
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)