Browse our anti-GIPR (GIPR) Antibodies

Human Gastric Inhibitory Polypeptide Receptor (GIPR) interaction partners

1. 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 (show HCAR3 Antibodies) Gs alpha subunit (show GNAS Antibodies), here) both at plasma membrane and in endosomes; recombinant proteins expressed in HEK293 cells were used in these studies.

2. GIPR overexpression does not appear to affect acromegalic patients' clinical features

3. Study shows the internalization of GIPR involving clathrin-coated pits, AP-2 (show GTF3A Antibodies) and dynamin (show DNM1 Antibodies) and its subsequent intracellular trafficking. GIP (show GIP Antibodies) stimulates a rapid robust internalization of the GIPR, the major part being directed to lysosomes.

4. The common variant rs10423928 in the GIPR gene is associated with increased risk of stroke in patients with type 2 diabetes.

5. 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.

6. The potential future role of gastric inhibitory peptide (GIP (show GIP Antibodies)) receptors as molecular targets in neuroendocrine neoplasms may be dependent on the tumor grade.

7. Results show that GIPR undergoes trafficking between the plasma membrane and intracellular compartments of both GIP (show GIP Antibodies)-stimulated and unstimulated adipocytes.

8. GIPR is overexpressed in gastric and duodenal neuroendocrine tumors

9. 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.

10. GIPR promoter was hypomethylated in type 2 diabetic patients as compared to controls.

Mouse (Murine) Gastric Inhibitory Polypeptide Receptor (GIPR) interaction partners

1. 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.

2. Microarray analysis revealed that pregnancy-specific glycoprotein 17 (Psg17), a potential CD9 (show CD9 Antibodies)-binding partner, was significantly decreased in GIP (show GIP Antibodies) receptor-knockout (Gipr-/-) testes.

3. GIPR signaling in adipose tissue plays a critical role in high fat diet-induced insulin (show INS Antibodies) resistance and hepatic steatosis in vivo, which may involve IL-6 (show IL6 Antibodies) signaling.

4. Genetic deletion of both GLP-1 (show GCG Antibodies) and GIP (show GIP Antibodies) receptors reveals that they are required to maintain an adequate islet number in adulthood and to maintain normal beta cell responses to glucose.

5. Results suggest the beneficial effects of glucose-dependent insulinotropic polypeptide (show GIP Antibodies) on periodontal disease.

6. Gipr(-/-) offspring of mice exposed to high fat diet(HFD) during pregnancy/lactation became insulin (show INS Antibodies) resistant and obese and exhibited increased adipose tissue inflammation and decreased peripheral tissue substrate utilization after reintroduction of HFD.

7. Beta-cell Gipr KO mice exhibit lower levels of meal-stimulated insulin (show INS Antibodies) secretion, decreased expansion of adipose tissue mass and preservation of insulin (show INS Antibodies) sensitivity and decreased TCF1 (show HNF1A Antibodies) expression.

8. Gipr is expressed in healthy arteries, predominantly in endothelial cells.

9. 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

10. Functional GIP (show GIP Antibodies) receptors play a major role in islet compensatory response to high fat feeding in mice.

Golden Syrian Hamster Gastric Inhibitory Polypeptide Receptor (GIPR) interaction partners

1. Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin (show INS Antibodies) by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide (show GIP Antibodies))/GIP (show GIP Antibodies) receptor signaling.