ELISA/assay

Human glucocorticoid receptor-beta ELISA Kit

MBS721669

48-Strip-Wells

470 USD

ELISA Kit

Human glucocorticoid receptor-beta ELISA Kit

glucocorticoid receptor-beta

Human glucocorticoid receptor-beta ELISA Kit; glucocorticoid receptor-beta; glucocorticoid receptor-b; glucocorticoid receptor- glucocorticoid receptor-beta (Human)

glucocorticoid receptor isoform beta; Glucocorticoid receptor; glucocorticoid receptor; OTTHUMP00000160084; OTTHUMP00000160085; OTTHUMP00000222851; OTTHUMP00000222854; OTTHUMP00000222855; OTTHUMP00000222858; glucocorticoid nuclear receptor variant 1; nuclear receptor subfamily 3 group C member 1; nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor); Nuclear receptor subfamily 3 group C member 1

GR-beta

GR-b; GR-

NR3C1; NR3C1; GR; GCR; GRL; GCCR; GRL

GCR_HUMAN

Human

Sensitivity: The sensitivity in this assay is 0.1 ng/mL. Specificity: This assay has high sensitivity and excellent specificity for detection of GR-beta. No significant cross-reactivity or interference between GR-beta and analogues was observed.

Store all reagents at 2-8 degree C

Samples: Cell culture fluid & body fluid & tissue homogenate Serum or blood plasma

Human ELISA Kit

For Samples: Cell culture fluid & body fluid & tissue homogenate serum or blood plasma. Intended Uses: This GR-beta ELISA kit is intended for laboratory research use only and not for use in diagnostic or therapeutic procedures. The stop solution changes the color from blue to yellow and the intensity of the color is measured at 450 nm using a spectrophotometer. In order to measure the concentration of GR-beta in the sample, this GR-beta ELISA Kit includes a set of calibration standards. The calibration standards are assayed at the same time as the samples and allow the operator to produce a standard curve of Optical Density versus GR-beta concentration. The concentration of in the samples is then determined by comparing the O.D. of the samples to the standard curve. Principle of the Assay: The coated well immunoenzymatic assay for the quantitative measurement of GR-beta utilizes a polyclonal anti-GR-beta antibody and an GR-beta-HRP conjugate. The assay sample and buffer are incubated together with GR-beta -HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the GR-beta concentration since GR-beta from samples and GR-beta-HRP conjugate compete for the anti-GR-beta antibody binding site. Since the number of sites is limited, as more sites are occupied by GR-beta from the sample, fewer sites are left to bind GR-beta-HRP conjugate. Standards of known GR-beta concentrations are run concurrently with the samples being assayed and a standard curve is plotted relating the intensity of the color (O.D.) to the concentration of GR- beta . The GR- beta concentration in each sample is interpolated from this standard curve.

66528642

NP_001018661.1

NM_001020825.1

P04150

85,659 Da

Adipogenesis Pathway (198832); Androgen Receptor Signaling Pathway (198806); Circadian Clock Pathway (187173); FOXA2 And FOXA3 Transcription Factor Networks Pathway (137911); Gene Expression Pathway (105937); Generic Transcription Pathway (105938); Glucocorticoid Receptor Regulatory Network Pathway (138014); IL-2 Signaling Pathway (198885); Neuroactive Ligand-receptor Interaction Pathway (83053); Neuroactive Ligand-receptor Interaction Pathway (462)

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). [provided by RefSeq]

Function: Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE) and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation. Involved in nuclear translocation. Subunit structure: Heteromultimeric cytoplasmic complex with HSP90, HSP70, and FKBP5 or another immunophilin, or the immunophilin homolog PPP5C. Directly interacts with UNC45A. Upon ligand binding FKBP5 dissociates from the complex and FKBP4 takes its place, thereby linking the complex to dynein and mediating transport to the nucleus, where the complex dissociates. By similarity. Binds to DNA as a homodimer, and as a heterodimer with NR3C2 or the retinoid X receptor. Binds STAT5A and STAT5B homodimers and heterodimers. Interacts with NRIP1, POU2F1, POU2F2 and TRIM28. Interacts with NCOA1, NCOA3, SMARCA4, SMARCC1, SMARCD1, and SMARCE1. By similarity. Interacts with several coactivator complexes, including the SMARCA4 complex, CREBBP/EP300, TADA2L and p160 coactivators such as NCOA2 and NCOA6. Interaction with BAG1 inhibits transactivation. Interacts with HEXIM1, PELP1 and TGFB1I1. Ref.16 Ref.17 Ref.18 Ref.21 Ref.28 Ref.30 Ref.31 Ref.32 Ref.53. Subcellular location: Cytoplasm. Nucleus. Note: Cytoplasmic in the absence of ligand, nuclear after ligand-binding.Isoform Beta: Nucleus. Note: Localized largely in the nucleus. Tissue specificity: Widely expressed. In the heart, detected in left and right atria, left and right ventricles, aorta, apex, intraventricular septum, and atrioventricular node as well as whole adult and fetal heart. Ref.20. Domain: Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal ligand-binding domain. Ref.14. Post-translational modification: Increased proteasome-mediated degradation in response to glucocorticoids.Phosphorylated in the absence of hormone; becomes hyperphosphorylated in the presence of glucocorticoid. The Ser-203-phosphorylated form is mainly cytoplasmic, and the Ser-211-phosphorylated form is nuclear. Transcriptional activity correlates with the amount of phosphorylation at Ser-211. Ref.27 Ref.33 Ref.34 Ref.35Sumoylated; this reduces transcription transactivation. Ref.26Ubiquitinated; restricts glucocorticoid-mediated transcriptional signaling. Polymorphism: Carriers of the 22-Glu-Lys-23 allele are relatively more resistant to the effects of GCs with respect to the sensitivity of the adrenal feedback mechanism than non-carriers, resulting in a better metabolic health profile. Carriers have a better survival than non-carriers, as well as lower serum CRP levels. The 22-Glu-Lys-23 polymorphism is associated with a sex-specific, beneficial body composition at young-adult age, as well as greater muscle strength in males. Involvement in disease: Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [. MIM:138040]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant. Ref.39 Ref.42 Ref.48 Ref.50 Ref.53. Miscellaneous: High constitutive expression of isoform beta by neutrophils may provide a mechanism by which these cells escape glucocorticoid-induced cell death. Up-regulation by proinflammatory cytokines such as IL8 further enhances their survival in the presence of glucocorticoids during inflammation.Can up- or down-modulate aggregation and nuclear localization of expanded polyglutamine polypeptides derived from AR and HD through specific regulation of gene expression. Aggregation and nuclear localization of expanded polyglutamine proteins are regulated cellular processes that can be modulated by this receptor, a well-characterized transcriptional regulator. Sequence similarities: Belongs to the nuclear hormone receptor family. NR3 subfamily.Contains 1 nuclear receptor DNA-binding domain.

48-Strip-Wells

470 USD

96-Strip-Wells

675