GCR_MOUSE Nr3c1 ELISA tesk kit
- Known as:
- GCR_MOUSE Nr3c1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17357
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- GCR_MOUSE Nr3c1 ELISA tesk kit
Related genes to: GCR_MOUSE Nr3c1 ELISA tesk kit
- Gene:
- NR3C1 NIH gene
- Name:
- nuclear receptor subfamily 3 group C member 1
- Previous symbol:
- GRL
- Synonyms:
- GR
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: GCR_MOUSE Nr3c1 ELISA tesk kit
Related articles to: GCR_MOUSE Nr3c1 ELISA tesk kit
- : Gestation is a period of significant biological plasticity where the intrauterine environment influences fetal development via "fetal programming". This study systematically reviews and meta-analyzes the association between genetic determinants-specifically the , , and genes, chosen for their pivotal role in the functional regulation and feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis-and stress reactivity during pregnancy. : Following PRISMA guidelines, a systematic search was conducted across PubMed, Scopus, and Web of Science, yielding an initial total of 1430 records. After removing duplicates and screening 669 studies, a total of 34 primary observational studies were included in the systematic review and qualitative synthesis. For the quantitative synthesis, 27 articles provided sufficient data, resulting in k = 39 independent effect sizes analyzed via a mixed-effects model to account for tissue-specific and cohort-specific outcomes. : Systematic analysis reveals that maternal psychosocial stress significantly correlates with hypermethylation, acting as a biological mediator for neonatal cortisol dysregulation and hippocampal volume reduction. The rs1360780 polymorphism emerged as a key moderator of structural vulnerability, showing a "double-hit" effect when combined with epigenetic alterations. Furthermore, the study identifies sex-specific susceptibility, with divergent placental trajectories for male and female fetuses. Meta-analytic estimates confirmed the robustness of these associations (Rosenthal Fail-Safe N = 431,000), despite a general trend toward statistical significance ( = 0.079) in heterogeneous cohorts. : The findings underscore a stable link between genetic determinants and prenatal stress reactivity. The interaction between molecular predisposition and environmental factors defines the health of the mother-infant dyad. These results advocate for a transition toward Precision Prenatal Medicine, integrating polygenic risk scores and epigenetic monitoring to implement early, targeted preventive interventions. - Source: PubMed
Publication date: 2026/04/25
Ioana Denisa SocolGeorge Socol FlaviusSorina Farcaș SimonaBogdan-Ionel DumitriuAlina-Iasmina DumitriuAndreea AntalAris BoartaDaniela IacobIoana Andreescu Nicoleta - To determine whether genetic variation in peroxisome proliferator-activated receptor gamma (PPARγ) is associated with mortality across corticosteroid exposure strata in pediatric septic shock. - Source: PubMed
Publication date: 2026/05/25
Bonnefil ValentinaStandage StephenLautz Andrew JStanski Natalja LHarmon KelliLahni PatrickFitzgerald Julie CSchwarz Adam JThomas Neal JHaileselassie BereketeabZingarelli BasiliaKaplan Jennifer MAtreya Mihir R - Androgenetic alopecia (AA) is a common condition that is characterized by androgen-induced follicular miniaturization and abnormal hair cycling, against which there are as yet no effective therapeutic interventions. The current study outlines the possibility of using stigmasterol (STR) as a therapeutic agent of AA, using geometry optimization, network pharmacology, molecular docking, and molecular dynamics (MD) simulations. Geometry optimization was done using the PM3 Hartree-Fock protocol, and the most stable conformation of STR was found with a total electronic energy of -164.36 au. The integrative gap analysis of target interactions presented sixty-three common genes in the target interaction between STR pharmacodynamics and AA pathogenesis. Ten core genes (AR, CDK4, ESR1, ESR2, HIF1A, MAPK3, MDM2, NR3C1, PGR, PPARG) were subsequently chosen in order to highlight the mechanistic nature of AA. Specifically, AR mediates androgenic signaling, which triggers the follicular miniaturization; ESR1 and ESR2 affect the cutaneous hair cycling and inflammatory cascades, and MAPK3 coordinates the inflammatory and apoptotic pathways. Docking studies revealed a strong binding of STR with all the hub genes, with the strongest binding affinity against MAPK3 (-9.1 kcal/mol) being observed compared to the binding energy of finasteride (-8.6 kcal/mol). Evidence of the thermodynamic stability of the STR-MAPK3 complex was found by MD simulations over 200 nanoseconds. Taken together, these results support the ability of STR to regulate a variety of AA-related mechanisms and thus predetermine it as one of the most promising natural therapeutic agents. However, further empirical confirmation is mandatory to unify the prospective application of STR in the clinical treatment of AA. - Source: PubMed
Publication date: 2026/05/23
Otuokere Ifeanyi EdozieNgwu Comfort MichaelIheanyichukwu Julian IbejiMac-Kalunta Onuchi MarygemNwadire Felix ChigozieNwankwo Chinedum IfeanyiEgbucha Joy NUfearoh Stella MbanyeakuChukwuemeka-Okorie Helen OUzoma Nwokoma EsomchiOluwaseyi Adeniji Moshood - Sensory experience refines neural circuits during critical periods of postnatal development. Although neuronal activity is known to orchestrate the circuit wiring that underlies this process, the environmental cues that restrain developmental plasticity as animals mature are less clear. Here we examine the experience-dependent maturation of the mouse primary visual cortex across postnatal development using paired single-cell transcriptomic and chromatin accessibility sequencing. In addition to identifying the activity-dependent gene programs that emerge within each cortical cell type, we find that light exposure drives astrocyte maturation through cell-type-specific recruitment of the glucocorticoid receptor (encoded by Nr3c1) to chromatin. Astrocyte glucocorticoid receptor signalling activates an extensive gene regulatory program that is partially conserved in human brain development and promotes maturation processes that may regulate critical period closure. Collectively, these findings reveal that astrocyte glucocorticoid receptor signalling restricts neuronal plasticity. Glucocorticoid regulation of astrocyte maturation may also contribute to the effects of early-life stress across the brain, and the disruption of this process may increase susceptibility to neuropsychiatric disease. - Source: PubMed
Publication date: 2026/05/20
Gegenhuber BrunoSonoda TakumaTraunmüller LisaDavis Christopher PKoren Shon AGriffith Eric CChen ChinfeiGreenberg Michael E - Chromatin conformational changes are key to gene regulation in the brain and have recently been shown to be regulated by super-enhancer RNAs (seRNAs). We examine the role of seRNAs in major depressive disorder (MDD) by profiling the prefrontal cortex from 25 MDD subjects and 25 matched non-psychiatric controls. Our analysis reveals 175 differentially expressed seRNAs, of which 140 are upregulated and 35 are downregulated. Our proximity mapping (±50 kb) links 94 seRNAs to nearby protein-coding genes, while long-range analysis (±500 kb) uncovered 584 seRNA-mRNA interaction pairs, most within 400 kb of genomic range. These interactions formed cis-regulatory hubs and hotspots, with notable pairs involving CEBPA, NR3C1, and DUSP1. Additionally, several genes are found to be co-regulated by distinct seRNAs. Spatial mapping confirms that many altered seRNAs are located near super-enhancer regions. Our results for the first time highlight seRNAs as key modulators of proximal and distal gene networks in MDD, offering novel insights and therapeutic avenues. - Source: PubMed
Publication date: 2026/05/19
Dwivedi YogeshRoy Bhaskar