GCGR/CRE Luciferase Reporter HEK293 Cell Line
GCGR/CRE Luciferase Reporter HEK293 Cell Line is a HEK293 cell line that expresses the firefly luciferase reporter, under the control of the cAMP response element (CRE), and human GCGR (Glucagon receptor; NM_000160.5). Activation of GCGR in these cells can be monitored by measuring luciferase activity.
This cell line was functionally validated with the agonists Glucagon and Retatrutide.
Figure 1. Example of the mechanism of action of GCGR/CRE Luciferase Reporter HEK293 Cell Line when treated with glucagon.
Binding of glucagon to GCGR triggers the activation of adenylyl cyclase and results in an increase of cAMP in the cells. Protein kinase A is activated, allowing the activation of the CRE promoter and luciferase production. Luciferase activity is thus proportional to GCGR binding to its agonists.
Interested in screening and profiling inhibitors, blocking antibodies, or activators of GCGR without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening.
Purchase of this cell line is for research purposes only; commercial use requires a separate license. View the full terms and conditions.
Media Required for Cell Culture
| Name | Ordering Information |
| Thaw Medium 1 | BPS Bioscience #60187 |
| Growth Medium 1G | BPS Bioscience #79544 |
Materials Required for Cellular Assay
| Name | Ordering Information |
| GCGR agonist such as: Glucagon Retatrutide |
R&D System #6927 MedChemExpress #HY-P3506 |
| Opti-MEM I Reduced Serum Medium | ThermoFisher #31985-070 |
| ONE-Step™ Luciferase Assay System | BPS Bioscience #60690 |
| Luminometer |
The cell line has been screened to confirm the absence of Mycoplasma species.
The glucagon receptor (GCGR) belongs to the Class B1 family of G protein-coupled receptors (GPCR family). Along with GLP-1R (glucagon-like peptide 1 receptor) and GIPR (gastric inhibitory polypeptide receptor), it is one of the critical receptors that regulate glucose homeostasis. Glucagon, the ligand of GCGR, increases insulin secretion via GCGR and GLP-1R in pancreatic β cells, although GLP-1R is the main insulin-promoting receptor. In addition, it has been shown that glucagon enhances hepatic lipid metabolism and reduces food intake in rodents and humans. More recently, encouraging clinical results from a triple-hormone-receptor agonist, Retatrutide, and several GLP-1R/GCGR dual agonists, suggest that GCGR could be a promising co-stimulating target for type 2 diabetes and obesity.
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