HEK293 Sus scrofa GIPR Stable Cell
Item | Cat# | Price |
Stable Cell Line | SNB-G-0103N | $19,800 |
Compound Testing Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
The Gastric Inhibitory Polypeptide Receptor (GIPR) is a class B G protein-coupled receptor (GPCR) that mediates the physiological actions of the incretin hormone GIP, primarily involved in glucose homeostasis and lipid metabolism. GIPR is predominantly expressed in pancreatic β-cells, adipose tissue, and the central nervous system, where it plays a key role in enhancing insulin secretion in response to nutrient intake.
Screeningbio’s Sus scrofa GIPR cell line stably expresses the full-length, non-tagged Sus scrofa GIPR in HEK293 cells. Upon activation by GIP or other agonists, the receptor couples to Gs proteins, resulting in an increase in intracellular cAMP levels, enabling quantitative assessment of GIPR activation in various functional assays.
Product Specifications
Target Type | GPCR |
Species | Sus scrofa |
HGNC Symbol | GIPR |
Accession Number | XM_021094578.1 |
Parental Line | HEK293 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
Target Background
The gastric inhibitory polypeptide receptor (GIPR), also known as the glucose-dependent insulinotropic polypeptide receptor, is a class B G-protein-coupled receptor (GPCR) that mediates the actions of the incretin hormone GIP. GIPR is highly expressed in pancreatic β-cells and adipose tissue, with additional expression in the gastrointestinal tract, bone, adrenal cortex, and central nervous system. This distribution underlies its diverse physiological functions in glucose regulation, lipid metabolism, and bone remodeling.
Upon nutrient ingestion, GIP is secreted from intestinal K-cells and activates GIPR, leading to coupling with Gs proteins, stimulation of adenylate cyclase, and elevation of intracellular cAMP. In pancreatic β-cells, this signaling enhances glucose-dependent insulin secretion and promotes β-cell proliferation and survival. In adipocytes, GIPR activation facilitates lipid uptake and storage, while in bone it contributes to anabolic effects on osteoblasts. Recent studies also suggest a role for GIPR in appetite regulation and energy expenditure through central mechanisms.
Pharmacologically, GIPR has emerged as an important target in metabolic disease. While early efforts to develop GIPR agonists showed modest effects in type 2 diabetes, the development of dual GLP-1R/GIPR agonists such as tirzepatide has demonstrated superior efficacy in improving glycemic control and inducing weight loss compared to GLP-1R agonists alone. Conversely, GIPR antagonism is under exploration for obesity and insulin resistance, highlighting the complex biology of this receptor. With its multifaceted influence on insulin secretion, adiposity, and skeletal health, GIPR remains a significant focus of incretin-based drug discovery and translational research.