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Opn4m2 labeling shows nuclear localization, which did not change in response to light. opn4m1, opn4m2, gr, per1b, and cry1b presented an oscillatory profile of expression in LD condition. In both DD and LD condition, dexamethasone (DEX) treatment shifted the peak expression of per1b and cry1b transcripts
GR agonists enhanced, whereas GR loss diminished, Hematopoietic stem and progenitor cell formation.
Two distinct gene clusters were found that were regulated by GRalpha: one that was regulated by GRalpha under basal conditions (presence of endogenous cortisol only), and one that was regulated upon increased activation of GRalpha.
We suggest that GR controls a gene network required for visual adaptation in the zebrafish retina and potentially integrates neuroendocrine and sensory responses to environmental changes.
This study demonistrated that disruption of GR causes a syndrome in adult zebrafish that resembles an affective disorder.
GR signaling is essential for zebrafish muscle development
The maternal gr transcript and protein participate in the maternal programming of zebrafish development.
The present study demonstrates that in zebrafish a GR isoform exists that diverges from the canonical zebrafish GR at the same position as human GRbeta from human GRalpha.
This work provides new findings inglucocorticoid (GC) field by bringing novel understanding on how GR integrates plasma membrane, allowing GC membrane-initiated signaling that differs in presence of GnRH to disrupt GnRH-dependent signaling and luteinizing hormone secretion.
The present study demonstrates the important role of GR in the regulation of the inflammatory responses and neurotrophic BDNF/TrkB signaling pathway in acute ischemic brain injuries in adult mice, revealing a new insight into the pathogenesis and therapeutic potential in acute ischemic strokes.
Absence of the GR significantly impairs fracture healing associated with a defective cartilage-to-bone transition.
Glucocorticoid receptor positively regulates transcription of FNDC5 in the liver.
this study shows that selective ablation of GR in noradrenergic neurons does not affect fundamental properties of peritoneal leukocytes
Data (including data from studies in knockout/transgenic mice) suggest that, under hypoxic conditions, muscle atrophy and elevated gene expression of ubiquitin proteasomal system-associated enzymes are mostly independent of glucocorticoid/Nr3c1 signaling.
We propose that the GC-induced mitochondrial accumulation of Bax and the interaction between the GR and Bim, Bcl-xL and Bak could play a role in the regulation of thymocyte apoptosis.
The potentiation of RANKL induced CTX release by dexamethasone was significantly less in bone marrow macrophage cells from mice with conditional knockout of the osteoclastic glucocorticoid receptor and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor.
These data establish SUMO conjugation as a novel regulatory mechanism in the Hsp90 cochaperone activity of FKBP51 with a functional impact on GR signaling in a neuronal context.
These results together suggested that ERK1 phosphorylation plays a critical role in regulating GR beta expression and hydrocortisone-induce GR phosphorylation at Ser220, which is critical for the anti-apoptotic effects hydrocortisone on hepatic ischemia-reperfusion injury.
GR signaling in macrophages, playing a crucial role in tissue-repairing mechanisms, could be a potential therapeutic target during wound healing after ischemic myocardial injury
a significant protein-protein interaction between GR and CHOP, (GR-CHOP heterocomplex formation) under endoplasmic reticulum stress conditions, is reported.
This study identifies an endocrine developmental axis in which fetal GR primes the activity of PPARalpha in anticipation of the sudden shifts in postnatal nutrient source and metabolic demands.
we propose that cell type-specific regulation by GR preferentially occurs via distal enhancers, whose chromatin accessibility is typically cell type-specific, whereas ubiquitous target gene regulation is more likely to result from binding to promoter regions, which are often accessible regardless of cell type examined.
Skin differentiation is impaired, and both apoptosis and cell proliferation are augmented in the absence of p23; the consequences are a severe thinning of the stratum corneum and reduced numbers of hair follicles. Since the phenotype of p23-null embryos is strikingly similar to that of embryos lacking the glucocorticoid receptor, a paradigmatic Hsp90-p23 client protein, we investigated glucocorticoid signaling.
REV-ERBalpha binds to the C-terminal portion and GR to the N-terminal portion of HSP90alpha and HSP90beta, a chaperone responsible for the activation of proteins to ensure survival of a cell.
These results clarify the role of GR in adipogenesis.
glucocorticoids profoundly alter corneal epithelial gene expression and many of these changes likely impact both wound healing and epithelial cell barrier function.
Phospho-AMPK is a molecular switch able to cooperate with glucocorticoid receptors and Ppar-alpha at the chromatin level, a novel adaptation mechanism to prolonged fasting.
Our data demonstrate that adipocyte-specific ablation of Gr in vivo may affect the adipose tissue function but not its expansion during a high calorie diet.
Bcl1 G/G polymorphism of glucocorticoid receptor gene is associated with bronchial asthma complicated by obesity.
topical mevastatin accelerates wound closure by promoting epithelialization via multiple mechanisms: modulation of GR ligands and induction of the long noncoding RNA Gas5, leading to c-Myc inhibition.
alpha-Viniferin (KCV) inhibits the activation of glucocorticoid receptor (GR) signaling pathway in non-androgen-dependent Prostate cancer (PCa) cells. KCV induces cancer cell apoptosis through AMP-Activated Protein Kinases-mediated activation of autophagy, and inhibits GR expression in castration-resistant prostate cancer(CRPC).
The genotypes for the NR3C1 polymorphisms in patients and controls were distributed as follows: rs6191 TT 37 : 56, GT 178 : 36, GG 332 : 609; rs6196 AA 483 : 905, AG 66 : 118, GG 2 : 4; rs10482614 GG 493 : 916, AG 61 : 108, AA 1 : 4; and rs72557310 AG 27 : 65, GG 3 : 0, AA 525 : 964. There were no significant differences in genotype frequency or in allele distributions between cases and controls.
Polymorphisms in NR3C1 gene is associated with sensitivity to glucocorticoids and it may contribute to the glucose abnormality for Acute Lymphoblastic Leukemia.
NR3C1 methylation moderates the effect of maternal support during stress on anxious attachment development 18 months later. More stressed children who experienced less maternal support reported increased anxious attachment when their NR3C1 gene was highly methylated. This effect could not be explained by children's level of psychopathology.
Meta-analysis showed that homozygous mutation of NR3C1 rs41423247 was associated with Depression.
This review focuses on the earlier findings on the pathophysiology of GR signaling and presents criteria facilitating identification of novel NR3C1 mutations in selected patients. [review]
study indicates that GR genetic polymorphisms may play a major role in the pathogenesis and development of systemic lupus erythematosus
The BclI NR3C1 polymorphisms were significantly associated with asthma in adults. (Meta-analysis)
Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5.
There was no significant association between different genotypes and alleles of Glucocorticoid Receptor of rs6195, rs6189/rs6190 variants, and response to fluoxetine (p=0.213 and 0.99, respectively).
NR3C1 gene polymorphisms are significantly associated with the response to glucocorticoids.
There is no clear evidence that the analysed NR3C1 allelic variants confer a risk for developing systemic autoimmune diseases although the minor G allele of rs41423247 may be protective among Caucasians (review and meta-analysis).
Analyses demonstrated a trend in the association between maternal trait anxiety and depression symptoms with placental gene expression of NR3C1. We found a significant interaction with maternal ethnicity. In Caucasians only, prenatal trait anxiety and depressive symptoms were associated with an increase in placental NR3C1 expression, and prenatal life events were associated with a down regulation of HSD11B2
We genotyped 10 single nucleotide polymorphisms (SNPs) on the NR3C1 gene (rs10482682, rs33389, rs10482633, rs10515522, rs2963156, rs4128428, rs9324918, rs41423247, rs6189, rs10052957).Haplotype analyses revealed significant effects of NR3C1 (p = 0.011) on cortisol stress response. Neither NR3C1 haplotype nor NR3C2 haplotype was associated with reasoning abilities.
In this study, we described the cellular localization of the glucocorticoid receptor in the human adult and fetal testis and provided evidence of an association between semen quality and a genetic polymorphism BclI (rs41423247) in the NR3C1 gene.
Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers.
children with early onset maltreatment evidence significant hypermethylation compared to nonmaltreated children. Also, hypermethylation of NR3C1 is linked with a number of negative child outcomes including greater emotional lability-negativity, higher levels of ego undercontrol, more externalizing behavior, and greater depressive symptoms.
This study reveals the role of GR in muscle fiber inhibition on intramuscular adipocytes, and identifies myostatin as a muscle-derived modulator for adipose GR level.
These results indicate that myostatin mediates maternal low protein diet-induced growth retardation, through epigenetic regulation involving FoxO3 and glucocorticoid receptor binding to its promoter.
Data indicate that higher hepatic glucocorticoid receptor (GR) expression in EHL piglets attributes mainly to the enhanced transcription of GR promoter 1-9/10 from breed-specific interaction of p53 and specificity protein 1 (Sp1).
Tissue specificities, gene expression and induction responsiveness of the porcine NR3C1 gene.
role in the breed-dependent regulation of mitochondrial genes in the liver of newborn piglets
Cloning and dna sequence analysis of the upstream flanking region of the NR3C1 gene in the domestic pig.
Effects of age, weaning and/or social isolation on the expression of genes regulating glucocorticoid response [glucocorticoid receptor).
Glucocorticoid Receptor protein expression in granulosa cells was higher in cysts from animals with spontaneous cystic ovarian disease and adrenocorticotropic hormone-induced cystic ovarian disease than in tertiary follicles from control animals.
Exposure to follicular fluid transiently increased the transcript levels of IL8 and PTGS2, and decreased the expression of SOD2, GPX3, DAB2, and NR3C1. TNF and IL6 levels were also decreased while those of NAMPT were unaffected.
Bayesian image analysis of dexamethasone and shear stress-induced glucocorticoid receptor intracellular movement
investigation of gene expression for GR, 11HSD1, and 11HSD2 in granulosa cells and theca interna layers during follicular maturation and atresia: expression of GR was largely unchanged during follicular maturation
Our results underscore a critical role for central and peripheral GR signaling in the regulation of plasma cortisol levels during stress in fish.
The E domain of the trout receptors are not involved in the nucleocytoplasmic localization of naive trout GRs, but the A/B domain, especially if linked to the corresponding trout CD region, plays a pivotal role in the cellular distribution pattern.
This gene encodes glucocorticoid receptor, which can function both as a transcription factor that binds to glucocorticoid response elements in the promoters of glucocorticoid responsive genes to activate their transcription, and as a regulator of other transcription factors. This receptor is typically found in the cytoplasm, but upon ligand binding, is transported into the nucleus. It is involved in inflammatory responses, cellular proliferation, and differentiation in target tissues. Mutations in this gene are associated with generalized glucocorticoid resistance. Alternative splicing of this gene results in transcript variants encoding either the same or different isoforms. Additional isoforms resulting from the use of alternate in-frame translation initiation sites have also been described, and shown to be functional, displaying diverse cytoplasm-to-nucleus trafficking patterns and distinct transcriptional activities (PMID:15866175).
, nuclear receptor subfamily 3, group C, member 1
, glucocorticoid receptor 1
, nuclear receptor subfamily 3 group C member 1
, glucocorticoid nuclear receptor variant 1
, glucocorticoid receptor alpha
, glucocorticoid receptor variant P
, glucocorticoid receptor variant beta
, glucocorticoid receptor variant gamma