| RQP71346 | |
| I. Background | |
The gastric inhibitory polypeptide receptor (GIP-R), also known as the glucose-dependent insulinotropic polypeptide receptor,which was originally identified as an activity in gut extracts that inhibited gastric acid secretion and gastrin release, but subsequently was demonstrated to stimulate insulin release in the presence of elevated glucose. Mice lacking this gene exhibit higher blood glucose levels with impaired initial insulin response after oral glucose load. Defect in this gene thus may contribute to the pathogenesis of diabetes. | |
| II. Introduction | |
| Host Cell: | HEK293 |
| Stability: | 20 passages(in-house test, that not means the cell line will be instable beyond the passages we tested.) |
| Freeze Medium: | 90% FBS+10% DMSO |
| Culture Medium: | DMEM +10%FBS+2ug/ml puromycin+200ug/ml hygromycin |
| Mycoplasma Status: | Negative |
| Storage: | Liquid nitrogen immediately upon delivery |
| Transducer: | Gs |
| Ⅲ. Description of Host Cell Line | |
| Organism: | Human |
| Tissue: | Embryonic kidney |
| Morphology: | Epithelial |
| Growth Properties: | Adherent |
| Ⅳ. Representative Data | |
Figure 1. Recombinant GIPR/CRE-Luc/HEK293 stably expressing human GIPR.
Figure 2. GIPR/CRE Reporter - HEK293 Recombinant Cell Line (C37). | |
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