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GIPR 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. Additionally we are shipping GIPR Antibodies (174) and GIPR Proteins (4) and many more products for this protein.
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Study shows the internalization of GIPR involving clathrin-coated pits, AP-2 (show GTF3A ELISA Kits) and dynamin (show DNM1 ELISA Kits) and its subsequent intracellular trafficking. GIP (show GIP ELISA Kits) stimulates a rapid robust internalization of the GIPR, the major part being directed to lysosomes.
The common variant rs10423928 in the GIPR gene is associated with increased risk of stroke in patients with type 2 diabetes.
Body mass index change for the A/T+A/A in GIPR genotypes was significantly higher than that for the T/T genotype. rs10423928 may predict weight gain in schizophrenia.
The potential future role of gastric inhibitory peptide (GIP (show GIP ELISA Kits)) receptors as molecular targets in neuroendocrine neoplasms may be dependent on the tumor grade.
Results show that GIPR undergoes trafficking between the plasma membrane and intracellular compartments of both GIP (show GIP ELISA Kits)-stimulated and unstimulated adipocytes.
GIPR is overexpressed in gastric and duodenal neuroendocrine tumors
GIPR expression was downregulated in subcutaneous adipose tissue from obese patients and correlated negatively with body mass index, waist circumference, systolic blood pressure, and glucose and triglyceride levels.
GIPR promoter was hypomethylated in type 2 diabetic patients as compared to controls.
This study demonstrates an association between a functional GIPR polymorphism Glu354Gln (rs1800437) and Bone mineral density and fracture risk.
Compared with the current treatment standard SSTR2 (show SSTR2 ELISA Kits), GIPR has only somewhat lesser absolute gene expression in tumor tissue but much lesser expression in normal tissue, making it a promising new target for neuroendocrine tumor imaging and therapy.
Gipr(-/-) offspring of mice exposed to high fat diet(HFD) during pregnancy/lactation became insulin (show INS ELISA Kits) resistant and obese and exhibited increased adipose tissue inflammation and decreased peripheral tissue substrate utilization after reintroduction of HFD.
Beta-cell Gipr KO mice exhibit lower levels of meal-stimulated insulin (show INS ELISA Kits) secretion, decreased expansion of adipose tissue mass and preservation of insulin (show INS ELISA Kits) sensitivity and decreased TCF1 (show HNF1A ELISA Kits) expression.
Gipr is expressed in healthy arteries, predominantly in endothelial cells.
These data highlighted the importance of intact GIPR signalling and dietary composition in modulating memory and learning, and hippocampal pathways involved in the maintenance of synaptic plasticity
Functional GIP (show GIP ELISA Kits) receptors play a major role in islet compensatory response to high fat feeding in mice.
our data demonstrate that the expression of GLP-1R (show GLP1R ELISA Kits) and GIPR is regulated by glucose concentrations in MC3T3-E1 cells undergoing differentiation induced by BMP-2 (show BMP2 ELISA Kits).
Structural and pharmacological characterization of novel potent and selective monoclonal antibody antagonists of glucose-dependent insulinotropic polypeptide receptor.
a role of the adipocyte GIPr in nutrient-dependent regulation of body weight and lean mass, but it does not support a direct and independent role for the adipocyte or beta-cell GIPr in promoting adipogenesis.
Gipr is essential for adrenal steroidogenesis and links high fat (HF) feeding to increased levels of corticosterone, reduced glucocorticoid levels do not significantly contribute to the enhanced metabolic phenotypes in HF-fed Gipr(-/-) mice.
Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin (show INS ELISA Kits) by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide (show GIP ELISA Kits))/GIP (show GIP ELISA Kits) receptor signaling.
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.
gastric inhibitory polypeptide receptor
, glucagon receptor
, gastric inhibitory polypeptide receptor-like
, glucose-dependent insulinotropic polypeptide receptor
, gastric inhibitory peptide receptor