GIPR/CRE Luciferase Reporter HEK293 Cell Line
GIPR/CRE Luciferase Reporter HEK293 Cell Line is an engineered HEK293 cell line expressing firefly luciferase under the control of cAMP response element (CRE), and human GIPR (Gastric Inhibitory Polypeptide receptor; NM_000164.4). Activation of GIPR in these cells can be monitored by measuring luciferase activity.
The functionality of the GIPR/CRE Luciferase Reporter HEK293 Cell Line was validated in dose-response assays using the agonists gastric inhibitory peptide (GIP), Tirzepatide, and Retatrutide. These agonists induce luciferase activity in a dose-dependent manner as depicted in Figure 1.
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Figure 1. Illustration of the mechanism of action in the GIPR/CRE Luciferase Reporter HEK293 Cell Line.
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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 |
Gastric Inhibitory Peptide (GIP), human | Genscript #RP10795 |
Tirzepatide hydrochloride | MedChemExpress #HY-P1731 |
Retatrutide | MedChemExpress #HY-P3506 |
Opti-MEM Reduced Serum Medium (Assay Medium) | ThermoFisher #31985-070 |
ONE-Step™ Luciferase Assay System | BPS Bioscience #60690 |
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The cell line has been screened to confirm the absence of Mycoplasma species.
The gastric inhibitory polypeptide receptor (GIPR), also known as glucose-dependent insulinotropic polypeptide receptor, belongs to the Class B1 G protein-coupled receptor (GPCR) family. GIPR is primarily found in the β-cells of the pancreas and serves as a receptor for the gastric inhibitory polypeptide (GIP) hormone. As one of the incretin hormones, GIP modulates glucose metabolism by stimulating the pancreatic β-cells to release insulin. Since GIPR/GLP-1R heterodimerization regulates GLP-1R signaling, dual agonists that bind both GIPR and GLP-1R have shown promising clinical efficacy for treating type II diabetes mellitus (T2DM) and obesity.
Yang B., et al., 2022 Molecular Metabolism 66: 101638