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 (Montrer YAP1 Anticorps) was the downstream effector of GPR4 signaling. Extracellular pH modulates the osteogenic responses of BMSCs by regulating the proton-sensing GPR4-YAP (Montrer YAP1 Anticorps) pathway.

2. These results suggest that zOGR1, but not GPR4, is also a metal-sensing G-protein-coupled receptor (Montrer ADRA1A Anticorps) in addition to a proton-sensing G-protein-coupled receptor (Montrer ADRA1A Anticorps), 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 (Montrer DDIT3 Anticorps) 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 (Montrer NOTCH1 Anticorps), a function that may be important for physiological and pathological angiogenesis.

6. GPR4 induces angiogenesis via GPR4-induced p38 (Montrer CRK Anticorps)-mediated IL6 (Montrer IL6 Anticorps), IL8 (Montrer IL8 Anticorps) and VEGFA (Montrer VEGFA Anticorps) 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 (Montrer RAPGEF3 Anticorps) 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 (Montrer ADRA1A Anticorps) by which LPC (Montrer PCSK7 Anticorps) signals proinflammatory activities.

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

1. GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP (Montrer DDIT3 Anticorps) expression.

2. Collectively, these results posit the acid sensor GPR4 as a novel component of central blood pressure control through interactions with the renin (Montrer REN Anticorps)-angiotensin system.

3. knockdown of a proton-sensing G protein-coupled receptor (Montrer GPR34 Anticorps) GPR4 markedly reduced CHOP (Montrer DDIT3 Anticorps) expression and endothelial cell apoptosis after hypoxia exposure.

4. The results indicate that through the G12 (Montrer TCF3 Anticorps)/13/Rho signaling pathway GPR4 modulates focal adhesion dynamics and reduces cell spreading and membrane ruffling.

5. The data identify GPR4 and TASK-2 (Montrer KCNK5 Anticorps) as distinct, parallel, and essential central mediators of respiratory chemosensitivity.

6. These results suggested that, at least in part, RANKL (Montrer TNFSF11 Anticorps) expression by osteoblasts in an acidic environment was mediated by cAMP/PKA signaling resulting from GPR4 activation.

7. GPR4 modulates glucose homeostasis by increasing insulin (Montrer INS Anticorps) sensitivity.

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

9. findings suggest that GPR4 activation by an acidic pH inhibits tumor cell migration and invasion, and the Rho GTPase (Montrer RACGAP1 Anticorps) is at least partly responsible for this phenotype

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