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The recombinant antibody against GIPR was produced using the Recombinant Human GIPR protein as the immunogen. This antibody exists as a non-conjugated isotype hIgG4, Affinity-chromatography purified. This antibody has been validated on ELISA.
The recombinant antibody against GIPR was produced using the Recombinant Human GIPR protein as the immunogen. This antibody exists as a non-conjugated isotype hIgG4, Affinity-chromatography purified. This antibody has been validated on ELISA.
$350.00
| Cat.No | ADC-56372A | Clonality | Monoclonal |
|---|---|---|---|
| Target Name | GIPR | Target Synonyms | Gastric inhibitory polypeptide receptor, GIPR |
| Form | Liquid | Species Reactivity | Human, Macaca fascicularis |
| Isotype | hIgG4 | Storage Buffer | 0.01M PBS, 0.03% Proclin 300; Constituents: 50% Glycerol, PH 7.4 |
| Purification Method | Affinity-chromatography purified | Conjugate | Non-conjugated |
| Application | ELISA | Storage | Upon receipt |
| Immunogen Description | Recombinant Human GIPR protein | Target Species | Human |
|---|---|---|---|
| Immunogen Sequence | Complete sequences for the immunogen, target protein, and peptides are available upon request. | Uniprot ID | P48546 |
Uniprot Id
P48546
Target Species
Human
Target Name
GIPR
Target Full Name
Gastric inhibitory polypeptide receptor
Target Function
This is a receptor for GIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase.
Target Subcellular Location
Cell membrane; Multi-pass membrane protein.
Target Protein Families
G-protein coupled receptor 2 family
Target Research Area
Others
Target Synonyms
GIPR; Gastric inhibitory polypeptide receptor; GIP-R; Glucose-dependent insulinotropic polypeptide receptor
Target Background
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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