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Human B1R Reporter Assay Kit
Product Description and Product Data
This is an all-inclusive cell-based luciferase reporter assay kit targeting the the Human Bradykinin B1 Receptor Reporter Assay System (B1R). INDIGO’s B1R reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the B1R. In addition to B1R 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 B1R. 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 | GPCR | ||
| Species | Human | ||
| Receptor Form | Hybrid | ||
| Assay Mode | Activation, Inhibition | ||
| Kit Components |
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| Shelf Life | 6 months | ||
| Shipping Requirements | Dry Ice | ||
| Storage temperature | -80C |
Data
Target Background
This assay utilizes proprietary human cells that provide constitutive expression of the receptors that comprise the Bradykinin B1 Receptor (B1R).
Bradykinin receptors are class A G protein-coupled receptors (GPCRs) that respond to kinin peptides. These receptors play an important role in mediating pain, increasing vascular permeability, and vasodilation. The Bradykinin receptor family includes two main subtypes: the Bradykinin B1 Receptor (B1R) which is synthesized de novo following tissue injury, and the constitutively expressed Bradykinin B2 Receptor (B2R).
Once synthesized following tissue injury, inflammation, or exposure to certain cytokines such as TNF-α, B1R can be activated by kinin metabolites lacking the C-terminal arginine such des-Arg9-bradykinin. Upon activation, B1R primarily signals through the Gq/11 pathway leading to calcium mobilization and an increase in intracellular calcium levels, resulting in an increase in vascular permeability. B1R is resistant to ligand-induced desensitization making it ideal for mediating long-term inflammatory and pain signals. Due to the many important roles played by B1R, dysregulation of the receptor can have pathological consequences such as chronic pain, cancer progression, and vascular inflammation.
Citations
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