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Human PGR Reporter Assay Kit
Product Description and Product Data
This is an all-inclusive cell-based luciferase reporter assay kit targeting the Human Progesterone Receptor (PGR). INDIGO’s PGR reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the PGR. In addition to PGR Reporter Cells, this kit provides two optimized media for use during cell culture and in diluting the user’s test samples, a reference agonist, Luciferase Detection Reagent, and a cell culture-ready assay plate. The principal application of this assay is in the screening of test samples to quantify any functional activity, either agonist or antagonist, that they may exert against human PGR. This kit provides researchers with clear, reproducible results, exceptional cell viability post-thaw, and consistent results lot to lot. Kits must be stored at -80C. Do not store in liquid nitrogen. Note: reporter cells cannot be refrozen or maintained in extended culture.
Features
Ready to Use Upon Receipt
- Includes All Needed Components
- Contains Transfected Reporter Cells
- Eliminates Cell Licensing Fees
- Clear, Reproducible Results
- Consistent Results Lot to Lot
Product Specifications
| Target Type | Nuclear Hormone Receptor | ||
| Species | Human | ||
| Receptor Form | Native | ||
| Assay Mode | Agonist, Antagonist | ||
| Kit Components |
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| Shelf Life | 6 months | ||
| Orthologs Available | Yes | ||
| Shipping Requirements | Dry Ice | ||
| Storage temperature | -80C |
Data
Target Background
INDIGO’s Human Progesterone Receptor (PGR) Reporter Assay System utilizes proprietary mammalian cells engineered to provide constitutive, high-level expression of human PGR (NR3C3), a ligand-dependent transcription factor.
INDIGO’s Reporter Cells include the luciferase reporter gene functionally linked to a PGR-responsive promoter. Thus, quantifying changes in luciferase expression in the treated reporter cells provides a sensitive surrogate measure of the changes in PGR activity. Luciferase gene expression occurs after ligand-bound PGR undergoes nuclear translocation, DNA binding, recruitment and assembly of the co-activators and accessory factors required to form a functional transcription complex, culminating in expression of the target gene. Unlike in vitro binding assays, and some other cell-based assay strategies, the readout from INDIGO’s reporter cells demands the same orchestration of all intracellular molecular interactions and events that can be expected to occur in vivo.
Citations
Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is an organophosphate flame retardant. The primary TDCPP metabolite, bis(1,3-dichloro-2-propyl) phosphate (BDCPP), is detectable in the urine of over 90 % of Americans. Epidemiological studies show sex-specific associations between urinary BDCPP levels and metabolic syndrome, which is an established risk factor for type 2 diabetes, heart disease, and stroke. We used a mouse model to determine whether TDCPP exposure disrupts glucose homeostasis. Six-week old male and female C57BL/6J mice were given ad libitum access to diets containing vehicle (0.1 % DMSO) and TDCPP resulting in the following treatment groups: 0 mg/kg/day, 0.02 mg/kg/day, 1 mg/kg/day, or 100 mg/kg/day. After being on the experimental diet for five weeks without interruption, body composition was analyzed, glucose and insulin tolerance tests were performed, and fasting glucose and insulin levels were quantified. TDCPP at 100 mg/kg/day caused male sex-specific adiposity, fasting hyperglycemia, and insulin resistance. TDCPP-induced modulation of nuclear receptor activation was investigated using an in vitro screen to identify potential mechanisms of metabolic disruption. TDCPP activated farnesoid X receptor (FXR) and pregnane X receptor (PXR), and inhibited the androgen receptor (AR). PXR target genes, but not FXR target genes, were upregulated in livers from mice exposed to 100 mg TDCPP/kg/day. Interestingly, PXR target genes were differentially expressed in livers from both males and females. It remains to be determined whether TDCPP-induced metabolic disruption occurs via modulation of nuclear receptor activity. Taken together, these studies build upon the association of TDCPP exposure and metabolic syndrome in humans by identifying sex-specific effects of TDCPP on glucose homeostasis in mice.
In an ongoing effort to study the environmental fate of endocrine-active steroid hormones, we report the formation of phenolic rearrangement products (3 and 4) with a novel 6,5,8,5-ring system following aqueous photolysis of dienogest (1) and methyldienolone (2). The structures were established by analysis of 2D NMR and HRMS data, and that of 3 was confirmed by X-ray diffraction analysis. These photoproducts exhibit progestogenic and androgenic activity, albeit with less potency than their parent compounds.
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