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Proton-sensing receptor coupled to several G-proteins, including G(s), G(13) and G(q)/G(11) proteins, leading to cAMP production.. Additionally we are shipping GPR4 Antibodies (37) and GPR4 Proteins (5) and many more products for this protein.
acidosis/GPR4-induced endoplasmic reticulum stress pathways in endothelial cells may regulate vascular growth and inflammatory response in the acidic microenvironment.
it was demonstrated that GPR4 affects ECs by regulating Notch1 (show NOTCH1 ELISA Kits), a function that may be important for physiological and pathological angiogenesis.
GPR4 induces angiogenesis via GPR4-induced p38 (show CRK ELISA Kits)-mediated IL6 (show IL6 ELISA Kits), IL8 (show IL8 ELISA Kits) and VEGFA (show VEGFA ELISA Kits) secretion at acidic extracellular pH in squamous cell carcinoma of the head and neck
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
acidosis/GPR4 signaling regulates endothelial cell adhesion mainly through the G(s)/cAMP/Epac (show RAPGEF3 ELISA Kits) pathway
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.
Endogenous GPR4 in endothelial cells may be a potential G protein-coupled receptor (show ADRA1A ELISA Kits) by which LPC (show PCSK7 ELISA Kits) signals proinflammatory activities.
GPR4, a close relative of OGR1 (show GPR68 ELISA Kits), also responds to pH changes, but elicits cyclic AMP (show APRT ELISA Kits) formation
sphingosylphosphorylcholine and lysophosphatidic acid are not the ligands for GPR4 and that this receptor may constitutively inhibit ERK1/2 (show MAPK1/3 ELISA Kits) activation
GPR4 and TDAG8 overexpression in human tumors plays a role in driving or maintaining tumor formation
Collectively, these results posit the acid sensor GPR4 as a novel component of central blood pressure control through interactions with the renin (show REN ELISA Kits)-angiotensin system.
knockdown of a proton-sensing G protein-coupled receptor (show GPR34 ELISA Kits) GPR4 markedly reduced CHOP (show DDIT3 ELISA Kits) expression and endothelial cell apoptosis after hypoxia exposure.
The results indicate that through the G12 (show TCF3 ELISA Kits)/13/Rho signaling pathway GPR4 modulates focal adhesion dynamics and reduces cell spreading and membrane ruffling.
The data identify GPR4 and TASK-2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.
These results suggested that, at least in part, RANKL (show TNFSF11 ELISA Kits) expression by osteoblasts in an acidic environment was mediated by cAMP/PKA signaling resulting from GPR4 activation.
GPR4 modulates glucose homeostasis by increasing insulin (show INS ELISA Kits) sensitivity.
Reduced pathological angiogenesis and tumor growth in mice lacking GPR4, a proton sensing receptor.
findings suggest that GPR4 activation by an acidic pH inhibits tumor cell migration and invasion, and the Rho GTPase (show RACGAP1 ELISA Kits) is at least partly responsible for this phenotype
These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.
Proton-sensing receptor coupled to several G-proteins, including G(s), G(13) and G(q)/G(11) proteins, leading to cAMP production.
G-protein coupled receptor 19
, G-protein coupled receptor 4