GLP-1R Antibody [DyLight 550] Summary
Immunogen |
A synthetic peptide made to an N-terminal extracellular portion of the human GLP1R protein (between residues 100-200). [UniProt P43220] |
Localization |
Cell membrane |
Isotype |
IgG |
Clonality |
Polyclonal |
Host |
Rabbit |
Gene |
GLP1R |
Purity |
Immunogen affinity purified |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
- Immunocytochemistry
- Immunocytochemistry/ Immunofluorescence
- Immunohistochemistry
- Immunohistochemistry-Paraffin
- Microarray
- Simple Western
- Western Blot
|
Application Notes |
Optimal dilution of this antibody should be experimentally determined. |
Reactivity Notes
Rat reactivity reported in scientific literature (PMID: 26398375).
Packaging, Storage & Formulations
Storage |
Store at 4C in the dark. |
Buffer |
50mM Sodium Borate |
Preservative |
0.05% Sodium Azide |
Purity |
Immunogen affinity purified |
Notes
DyLight (R) is a trademark of Thermo Fisher Scientific Inc. and its subsidiaries.
Alternate Names for GLP-1R Antibody [DyLight 550]
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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