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anti-Human GIPR Antibodies:
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Human Polyclonal GIPR Primary Antibody for IHC (p) - ABIN4314158
Snook, Nelson, Dyck, Wright, Holloway: Glucose-dependent insulinotropic polypeptide directly induces glucose transport in rat skeletal muscle. in American journal of physiology. Regulatory, integrative and comparative physiology 2015
Show all 4 Pubmed References
Human Polyclonal GIPR Primary Antibody for IHC (p) - ABIN270972
Prasadan, Koizumi, Tulachan, Shiota, Lath, Paredes, Guo, El-Gohary, Malek, Shah, Gittes: The expression and function of glucose-dependent insulinotropic polypeptide in the embryonic mouse pancreas. in Diabetes 2011
Cow (Bovine) Polyclonal GIPR Primary Antibody for IHC (p) - ABIN4314159
Figueiredo, Antunes, Moreira, de Mello, Medeiros, Di Giunta, Lobão-Soares, Linhares, Lin, Mazzuco, Prediger, Walz: Glucose-dependent insulinotropic peptide receptor expression in the hippocampus and neocortex of mesial temporal lobe epilepsy patients and rats undergoing pilocarpine induced status epilepticus. in Peptides 2011
Human Polyclonal GIPR Primary Antibody for WB - ABIN6680704
Ussher, Campbell, Mulvihill, Baggio, Bates, McLean, Gopal, Capozzi, Yusta, Cao, Ali, Kim, Kabir, Seino, Suzuki, Drucker: Inactivation of the Glucose-Dependent Insulinotropic Polypeptide Receptor Improves Outcomes following Experimental Myocardial Infarction. in Cell metabolism 2018
Human Polyclonal GIPR Primary Antibody for FACS, IHC (p) - ABIN391714
Ugleholdt, Pedersen, Bassi, Füchtbauer, Jørgensen, Kissow, Nytofte, Poulsen, Rosenkilde, Seino, Thams, Holst, Holst: Transgenic rescue of adipocyte glucose-dependent insulinotropic polypeptide receptor expression restores high fat diet-induced body weight gain. in The Journal of biological chemistry 2011
SNPs in GIPR gene causes changes of secretion in hormones and adipokines in patients with obesity with type 2 diabetes
Study shows that there is sufficient evidence to confirm that gastric inhibitory polypeptide is an obesity-promoting factor in high fat diet conditions and that deletion of gastric inhibitory polypeptide receptor signaling causes resistance to diet-induced obesity.
an association between the GIPR rs2302382 polymorphism and type 2 diabetes mellitus in Egyptian patients.
Data suggest that GIPR (gastric inhibitory polypeptide receptor) is among the few GPCRs (G-protein-coupled receptors) which signal through G-proteins (GTP-binding protein Gs alpha subunit, here) both at plasma membrane and in endosomes; recombinant proteins expressed in HEK293 cells were used in these studies.
GIPR overexpression does not appear to affect acromegalic patients' clinical features
Study shows the internalization of GIPR involving clathrin-coated pits, AP-2 and dynamin and its subsequent intracellular trafficking. GIP 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) 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-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, 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.
Structural and pharmacological characterization of novel potent and selective monoclonal antibody antagonists of glucose-dependent insulinotropic polypeptide receptor.
no detectable effect (with an OR >2.1) of the variants in GCKR, GIPR, ADCY5 and VPS13C on the response to sulfonylurea treatment, indicating that these variants are not significantly contributing to the risk of SH in patients with T2D
Functional expression of a GIP receptor mutant lacking N-glycosylation is rescued by co-expressed wild type GLP1 receptor, which suggests formation of a GIP-GLP1 receptor heteromer.
Our prospective, observational study indicates that the type 2 diabetes risk by dietary intake of carbohydrate and fat may be dependent on GIPR genotype.
Most of the somatostatin receptor-negative neuroendocrine tumors and GLP-1 receptor-negative malignant insulinomas are GIP receptor positive.
GiprKO mice fed moderate high-fat diet did not display weight gain. On the other hand, GiprKO mice fed high carbohydrate (ST) showed weight gain and did not display obvious glucose intolerance. Glucose-induced insulin secretion was enhanced during intraperitoneal glucose tolerance tests and from isolated islets in both WT and GiprKO mice fed ST compared with those fed normal chow.
Glp1r/gipr double knockout mice have higher insulin clearance than WT mice, following intravenous injection of glucose. This suggests that incretin hormones reduce insulin clearance at physiological, nonstimulated levels.
The study provides evidence that the insulinotropic action of zfGIP in mammalian systems involves activation of both the GLP-1 and the GIP receptors but not the glucagon receptor
GIP stimulation induces a switch in GIPR recycling from a rapid endosomal to a slow trans-Golgi network (TGN) pathway. GPCR kinases and b-arrestin2 are required for this switch in recycling.
Microarray analysis revealed that pregnancy-specific glycoprotein 17 (Psg17), a potential CD9-binding partner, was significantly decreased in GIP receptor-knockout (Gipr-/-) testes.
GIPR signaling in adipose tissue plays a critical role in high fat diet-induced insulin resistance and hepatic steatosis in vivo, which may involve IL-6 signaling.
Genetic deletion of both GLP-1 and GIP receptors reveals that they are required to maintain an adequate islet number in adulthood and to maintain normal beta cell responses to glucose.
Results suggest the beneficial effects of glucose-dependent insulinotropic polypeptide on periodontal disease.
Gipr(-/-) offspring of mice exposed to high fat diet(HFD) during pregnancy/lactation became insulin 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 secretion, decreased expansion of adipose tissue mass and preservation of insulin sensitivity and decreased TCF1 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 receptors play a major role in islet compensatory response to high fat feeding in mice.
our data demonstrate that the expression of GLP-1R and GIPR is regulated by glucose concentrations in MC3T3-E1 cells undergoing differentiation induced by BMP-2.
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.
GIPR(dn) transgenic mice show a disturbed expansion of the endocrine pancreas, due to perturbed islet neogenesis.
GIP receptors play an important role in cognition, neurotransmission, and cell proliferation.
Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide)/GIP 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