anti-G Protein-Coupled Receptor 4 (GPR4) Anticorps

Human G Protein-Coupled Receptor 4 (GPR4) interaction partners

1. Proton-sensing GPR4 signaling mediated the proton-induced inhibitory effects on the osteogenesis of BMSCs. YAP was the downstream effector of GPR4 signaling. Extracellular pH modulates the osteogenic responses of BMSCs by regulating the proton-sensing GPR4-YAP pathway.

2. These results suggest that zOGR1, but not GPR4, is also a metal-sensing G-protein-coupled receptor in addition to a proton-sensing G-protein-coupled receptor, although not all metals that activate hOGR1 activated zOGR1.

3. GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression.

4. acidosis/GPR4-induced endoplasmic reticulum stress pathways in endothelial cells may regulate vascular growth and inflammatory response in the acidic microenvironment.

5. it was demonstrated that GPR4 affects ECs by regulating Notch1, a function that may be important for physiological and pathological angiogenesis.

6. GPR4 induces angiogenesis via GPR4-induced p38-mediated IL6, IL8 and VEGFA secretion at acidic extracellular pH in squamous cell carcinoma of the head and neck

7. The results suggested that GPR4 may play an important role in the development of epithelial ovarian carcinoma (EOC), and its overexpression might be required for the angiogenesis, tumor growth, and metastasis of EOC

8. acidosis/GPR4 signaling regulates endothelial cell adhesion mainly through the G(s)/cAMP/Epac pathway

9. The mutation of histidine residue at 79, 165, or 269 from the N-terminal of GPR4 to phenylalanine shifted the half-maximal effective concentration (EC(50)) of proton-induced signaling activities to the right, including cAMP accumulation.

10. Endogenous GPR4 in endothelial cells may be a potential G protein-coupled receptor by which LPC signals proinflammatory activities.

11. GPR4, a close relative of OGR1, also responds to pH changes, but elicits cyclic AMP formation

12. sphingosylphosphorylcholine and lysophosphatidic acid are not the ligands for GPR4 and that this receptor may constitutively inhibit ERK1/2 activation

13. GPR4 and TDAG8 overexpression in human tumors plays a role in driving or maintaining tumor formation

14. results identify sphingosylphosphorylcholine and its receptor, G protein-coupled receptor 4(GPR4), as critical regulators of the angiogenic potential of endothelial cells

15. GPR4 may play a critical role in the inflammatory responses activated by lysophosphatidylcholine

16. GPR4 in brain endothelial cells regulates monocyte transmigration.

17. lysophosphatidylcholine receptor G protein-coupled receptor 4 (GPK4) was expressed in YPEN-1 cells and triggered the cAMP/protein kinase A/cAMP response element-binding protein pathway, resulting in upregulation of adhesion molecules.

18. Previously postulated "ligand-independent" signaling of GPR4 is mediated through proton-sensing mechanisms.

Mouse (Murine) G Protein-Coupled Receptor 4 (GPR4) interaction partners

1. GPR4 deficiency reduces acute intestinal inflammation in a mouse colitis model. GPR4 gene expression is upregulated in inflamed mouse and human intestinal tissues.

2. GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression.

3. Collectively, these results posit the acid sensor GPR4 as a novel component of central blood pressure control through interactions with the renin-angiotensin system.

4. knockdown of a proton-sensing G protein-coupled receptor GPR4 markedly reduced CHOP expression and endothelial cell apoptosis after hypoxia exposure.

5. required for maintenance of normal acid-base homeostasis

6. The results indicate that through the G12/13/Rho signaling pathway GPR4 modulates focal adhesion dynamics and reduces cell spreading and membrane ruffling.

7. The data identify GPR4 and TASK-2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.

8. These results suggested that, at least in part, RANKL expression by osteoblasts in an acidic environment was mediated by cAMP/PKA signaling resulting from GPR4 activation.

9. GPR4 modulates glucose homeostasis by increasing insulin sensitivity.

10. Reduced pathological angiogenesis and tumor growth in mice lacking GPR4, a proton sensing receptor.

11. findings suggest that GPR4 activation by an acidic pH inhibits tumor cell migration and invasion, and the Rho GTPase is at least partly responsible for this phenotype

12. pH sensor with an important role in regulating acid secretion in the kidney collecting duct

13. These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.