Recombinant Human GIPR Protein, hFc Tag
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| Amount : | 50 µg |
| Content : | Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8% trehalose is added as protectants before lyophilization. |
| Storage condition : | Store at -20°C to -80°C for 12 months in lyophilized form. After reconstitution, if not intended for use within a month, aliquot and store at -80°C (Avoid repeated freezing and thawing). Lyophilized proteins are shipped at ambient temperature. |
| Uniprot ID : | P48546 |
| Alternative Name : | PGQTL2 |
Molecular Characterization: GIPR(Arg22-Gln138) hFc(Glu99-Ala330)
Molecular weight: The protein has a predicted molecular mass of 39.6 kDa after removal of the signal peptide. The apparent molecular mass of GIPR-hFc is approximately 35-55 kDa due to glycosylation.
Description: Recombinant Human GIPR Protein with C-terminal human Fc tag
This gene encodes a G-protein coupled receptor for gastric inhibitory polypeptide (GIP), 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.
Molecular weight: The protein has a predicted molecular mass of 39.6 kDa after removal of the signal peptide. The apparent molecular mass of GIPR-hFc is approximately 35-55 kDa due to glycosylation.
Description: Recombinant Human GIPR Protein with C-terminal human Fc tag
This gene encodes a G-protein coupled receptor for gastric inhibitory polypeptide (GIP), 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.
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