Predicted cross-reactivity based on sequence identity: Gorilla (100%), Marmoset (95%), Canine (89%), Hamster (89%), Rabbit (84%). Rat reactivity reported in scientific literature (PMID: 26041107). Mouse reactivity reported in scientific literature (PMID: 29275960).
Packaging, Storage & Formulations
Keep as concentrated solution. Aliquot and store at -20C or below. Avoid multiple freeze-thaw cycles.
0.1% Sodium Azide
Immunogen affinity purified
Product can be stored undiluted at 4C for up to 1 month.
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 Cushing'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 research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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