GLP-1R Antibody (197920) [Allophycocyanin/Cy7] Summary
Immunogen |
NS0 mouse myeloma cell line transfected with human GLP-1R Arg24-Ser463 Accession # NP_002053 |
Specificity |
Stains human GLP-1R transfectants but not irrelevant transfectants in flow cytometry. |
Isotype |
IgG2b |
Clonality |
Monoclonal |
Host |
Mouse |
Gene |
GLP1R |
Purity |
Protein A or G purified from hybridoma culture supernatant |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
|
Application Notes |
Optimal dilution of this antibody should be experimentally determined. For optimal results using our Tandem dyes, please avoid prolonged exposure to light or extreme temperature fluctuations. These can lead to irreversible degradation or decoupling. When staining intracellular targets, specific attention to the fixation and permeabilization steps in your flow protocol may be required. Please contact our technical support team at technical@novusbio.com if you have any questions. |
Packaging, Storage & Formulations
Storage |
Store at 4C in the dark. Do not freeze. |
Buffer |
PBS |
Preservative |
0.05% Sodium Azide |
Purity |
Protein A or G purified from hybridoma culture supernatant |
Alternate Names for GLP-1R Antibody (197920) [Allophycocyanin/Cy7]
Background
GLP1R, a Glucagon Receptor, has been suggested to affect the feelings of satiety or hunger, sensation of glucose levels, control of glucagon sensitivity of islets, and non insulin-dependent diabetes mellitus. Glucagon-like peptide 1 is an incretin hormone produced by enteroendocrine L-cells in the intestinal mucosa. The hormone is released in response to food intake and plays an important role in maintaining blood glucose homeostasis. Stimulation of the GLP-1R by endogenous hormone induces multiple complementary mechanisms, which together result in a lowering of circulating blood glucose levels. These mechanisms include receptor-mediated enhancement of glucose-induced insulin secretion from pancreatic -cells, inhibition of gastric emptying with a delay in the gastrointestinal resorption of nutrients, inhibition of glucagon secretion, and inhibition of food intake. Desensitization of GLP1R on pancreatic beta-cells is one of the causes of non insulin-dependent diabetes mellitus (NIDDM). GLP1R knockout mice are viable, develop normally, but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. Recently it has been shown that overexpression of glucagon-like peptide-1 receptor improves learning in rats (During et al. 2003). GLP1R has been reported in pancreas, brain, heart, kidney, lung, and stomach. ESTs have been isolated from kidney and skin libraries.
Limitations
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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