GCR_RAT Nr3c1 ELISA tesk kit
- Known as:
- GCR_RAT Nr3c1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17372
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- GCR_RAT Nr3c1 ELISA tesk kit
Related genes to: GCR_RAT 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
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- Many studies have focused on identifying specific biomarkers for the early diagnosis of non-traumatic osteonecrosis of the femoral head (NONFH). This systematic review aims to summarize biomarkers associated with the diagnosis and progression prediction of NONFH, thereby providing a molecular level foundation for clinical diagnosis and targeted treatment. - Source: PubMed
Publication date: 2026/09/21
Dong YaweiSun JigaoLi ShuwenZhang JiawenYan YanLi TaixianJia Yan - GPR55 has attracted attention for its anti-inflammatory, neuroprotective, and neurotransmitter-modulating properties, suggesting a role in mood regulation. Here, we aimed to clarify the contribution of GPR55 to emotional responses. - Source: PubMed
Publication date: 2026/09/03
García-Gutiérrez María SIllescas LucíaGasparyan AniManzanares Jorge - Cadmium (Cd) is a widespread environmental contaminant that has a detrimental impact on male reproductive toxicity (MRT) due to oxidative stress, endocrine imbalance, inflammation and cell death processes. Despite the known potential of melatonin (MLT) to ameliorate the adverse effects of Cd on MRT, the exact molecular mechanisms of such multistep action are still obscure. In this work, an integrated computational approach based on network pharmacology, protein-protein interaction (PPI) network analysis, molecular docking, MM-GBSA binding energy calculation, molecular dynamics (MD) simulation, and functional annotation was used for understanding of the molecular basis of MLT-mediated protection. Forty shared targets were found between MLT-related genes and MRT-related genes caused by Cd exposure. Ten hub genes (PTGS2, ESR1, MAPK8, EGFR, AR, NR3C1, PGR, CCND1, MMP9, and NFKB1) were selected based on network topology analysis. Functional annotation revealed that these targets are mostly involved in steroid hormone signaling, reproductive system development, transcription regulation, inflammatory signaling, and cancer pathways. Molecular docking identified that MAPK8 and PGR are the two best-binding proteins of MLT with docking scores of -7.783 and -6.830 kcal/mol, respectively and MM-GBSA binding energies of -66.10 and -63.63 kcal/mol, respectively. Further MD simulations over 300 ns proved to be successful in achieving a stable ligand-protein complex, maintaining structural stability, and stable binding during the course of the simulations. Taken together, these results indicate that MLT might operate via modulation of the oxidative stress-related, endocrine-related, and inflammation-related pathways simultaneously instead of operating through one specific target. - Source: PubMed
Publication date: 2026/09/10
Wanjari Uddesh RameshMukherjee Anirban GoutamJayaraman ManikandanPrabhu DhamodharanJeyaraman JeyakanthanMataghare Bhairav Chandroday - Obesity-associated adipose tissue dysfunction is a major contributor to metabolic disease. Although obesity is associated with increased glucocorticoid exposure, the role of glucocorticoid receptor (GR) signaling in mature adipocytes during obesity remains unclear. - Source: PubMed
Publication date: 2026/09/08
Wang HaoyuChen LingfengNie PengfeiZhang XinyiTan BaijiaLiu ChangqianZhang XinyueLu ShuangQiao NidanChen HaibingShao YikaiLi Qian - Glucocorticoids remain among the most widely prescribed immunosuppressive and anti-inflammatory agents worldwide, yet their clinical use is complicated by substantial inter-individual variability in both therapeutic response and adverse effects. Despite decades of clinical experience, glucocorticoid prescribing remains largely empirical, with limited integration of precision medicine approaches that could optimize therapeutic outcomes while minimizing toxicity. This review synthesizes current evidence on emerging precision approaches to glucocorticoid therapy across three key domains: pharmacogenomic determinants (including variants in NR3C1, FKBP5, CYP3A4/5, and ABCB1) that modulate immune cell responsiveness to glucocorticoids; pharmacokinetic variability and model-informed precision dosing strategies; and disease-specific biomarker-guided approaches across major immune-mediated conditions including respiratory diseases, rheumatologic conditions, inflammatory bowel disease, polymyalgia rheumatica, and critical illness. Genetic variants in glucocorticoid receptor signaling and drug metabolism pathways have suggested some associations with treatment response and adverse effects, although none are yet acknowledged as clinically actionable by consensus resources. Disease-specific immunological biomarkers including eosinophil counts, inflammatory cytokines, and pharmacodynamic endpoints suggest the promise of individualized dose optimization. Risk stratification for glucocorticoid-induced osteoporosis-mediated through OPG/RANKL signaling and monocyte-osteoclast crosstalk-incorporating both clinical factors and pharmacogenetic markers may facilitate targeted prevention strategies. The integration of pharmacogenomic testing, immune biomarker monitoring, and pharmacokinetic modeling represents an aspirational paradigm shift from empirical dosing to individualized immunomodulatory therapy. It should be acknowledged that, as of the time of writing, this precision framework remains largely investigational: routine clinical practice continues to rely predominantly on indication-specific regimens and empirical tapering protocols. This review is explicitly forward-looking, aiming to outline a research agenda for precision glucocorticoid therapy in immune-mediated diseases. - Source: PubMed
Publication date: 2026/08/24
Colina MatteoCampana Gabriele