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The antibody against GIPR was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 22-138 of human GIPR (NP_000155.1) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, ELISA.
The antibody against GIPR was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 22-138 of human GIPR (NP_000155.1) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, ELISA.
| Cat.No | ADA-08912A | Clonality | Polyclonal |
|---|---|---|---|
| Host Species | Rabbit | Target Name | GIPR |
| Target Synonyms | PGQTL2; GIPR | Form | Liquid |
| Species Reactivity | Human, Mouse, Rat | Isotype | IgG |
| Storage Buffer | 50% Glycerol, PBS with 0.02% sodium azide, pH7.3. | Purification Method | Affinity purification |
| Positive Samples | Rat brain, Rat heart, K-562, Mouse liver | Application | ELISA, WB, IHC-P |
| Immunogen Description | Recombinant fusion protein containing a sequence corresponding to amino acids 22-138 of human GIPR (NP_000155.1). | Target Species | Human |
|---|---|---|---|
| Immunogen Sequence | RAETGSKGQTAGELYQRWERYRRECQETLAAAEPPSGLACNGSFDMYVCWDYAAPNATARASCPWYLPWHHHVAAGFVLRQCGSDGQWGLWRDHTQCENPEKNEAFLDQRLILERLQ | 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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