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GASTRIC INHIBITORY POLYPEPTIDE REC. ANTIBODIES > GASTRIC INHIBITORY POLYPEPTIDE REC. POLYCLONAL ANTIBODY OPA1-15060
Anti-Gastric Inhibitory Polypeptide Rec. Polyclonal Antibody
Printable Datasheet
Synonyms:
GIP-R
Entrez Gene ID:
(Human) 2696
UniProt ID:
P48546
| Details | |
| Host / Isotype: | Rabbit / IgG |
| Class: | Polyclonal |
| Type: | Antibody |
| Species Reactivity: | Human (Hu) |
| Immunogen: | Synthetic peptide (KLH conjugated) to the N-terminus. |
| Ordering Information | ||||
| Pierce Anti-Gastric Inhibitory Polypeptide Rec. Polyclonal Antibody | ||||
| Product Number | Pkg. Size | Price | Purchase | |
| OPA1-15060 | 25 µg | $396.00 | ||
| Storage: | -20º C, Avoid Freeze/Thaw Cycles |
| Form: | 25 µg of antibody (1 mg/ml) in PBS, pH 7.7, with 0.01% sodium azide. |
| Applications | Dilution |
| Immunohistochemistry (Paraffin) (IHC (P)) | 1:100 -1:200 |
| Product Specific Information |
| OPA1-15060 detects the gastric inhibitory polypeptide receptor from human samples. OPA1-15060 has been successfully used in immunohistochemistry procedures. By immunohistochemistry, OPA1-15060 detects the gastric inhibitory polypeptide receptor in formalin fixed, paraffin embedded human tissues. The OPA1-15060 immunogen is a synthetic peptide (KLH conjugated) to the N-terminus. |
| General Information |
| GIPR, or Gastric Inhibitory Polypeptide Receptor, mediates GIP-induced secretion of insulin by pancreatic islet beta cells after a meal. GIP is a gastrointestinal peptide hormone of 42 aa that is released from duodenal endocrine K cells after absorption of glucose or fat. Stimulation of the GIPR on pancreatic cells activates adenylyl cyclase and mitogen-activated protein kinase, resulting in increased insulin secretion. Mice with a targeted mutation of GIPR have higher blood glucose levels with impaired initial insulin response after oral glucose load. Analysis of GIPR knockout mice suggest that GIPR defects may contribute to the pathogenesis of diabetes and obesity. Ectopic expression of functional GIPR and its coupling to steroidogenesis has been suggested to be the main cause of food-dependent Cushinga€(tm)s syndrome. Two isoforms of GIPR are produced by alternative splicing. GIPR expression has been reported in human bone, fetal adrenal, and pancreas. Little expression has been identified in normal adult adrenal, but overexpression of GIPR has been observed in the adrenal in food-dependent Cushing's syndrome. GIPR expression has been identified in rat brain, heart, pancreas, and small intestine. ESTs have been isolated from colon libraries. |
(This product is for In Vitro experimental use only.)
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