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Mouse PXR Reporter Assay Kit
Product Description and Product Data
This is an all-inclusive cell-based luciferase reporter assay kit targeting the Mouse Pregnane X Receptor (mPXR). INDIGO’s mPXR reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the mPXR. In addition to mPXR 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 mPXR. 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
Clear, Reproducible Results
- All-Inclusive Assay Systems
- Exceptional Cell Viability Post-Thaw
- Consistent Results Lot to Lot
Product Specifications
| Target Type | Nuclear Hormone Receptor, Nuclear Receptor Orthologs | ||
| Species | Mouse | ||
| Receptor Form | Hybrid | ||
| Assay Mode | Agonist, Antagonist | ||
| Kit Components |
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| Shelf Life | 6 months | ||
| Shipping Requirements | Dry Ice | ||
| Storage temperature | -80C |
Data
Target Background
Pregnane X Receptor also known as nuclear receptor subfamily 1, group I, member 2 (NR1I2) and SXR is a nuclear receptor that binds and is activated by variety of endogenous and xenobiotic compounds. PXR activates the transcription of multiple genes involved in the metabolism and secretion of potentially harmful xenobiotics, drugs, and endogenous compounds. Activated by the antibiotic rifampicin and various plant metabolites, such as hyperforin, guggulipid, colupulone, and isoflavones, its response to specific ligands is species-specific. PXR is activated by naturally occurring steroids, such as pregnenolone and progesterone and binds to a response element in the promoters of the CYP3A4 and ABCB1/MDR1 genes.
This assay product utilizes proprietary mammalian cells engineered to provide constitutive, high-level expression of the Mouse Pregnane X Receptor (nr1i2), a ligand-dependent transcription factor commonly referred to as PXR. PXR is also known as the Steroid and Xenobiotic sensing nuclear receptor (SXR).
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.
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