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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 (36) and many more products for this protein.
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GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP (show DDIT3 Proteins) expression.
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 Proteins), a function that may be important for physiological and pathological angiogenesis.
GPR4 induces angiogenesis via GPR4-induced p38 (show CRK Proteins)-mediated IL6 (show IL6 Proteins), IL8 (show IL8 Proteins) and VEGFA (show VEGFA Proteins) 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 Proteins) 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 Proteins) by which LPC (show PCSK7 Proteins) signals proinflammatory activities.
GPR4, a close relative of OGR1, also responds to pH changes, but elicits cyclic AMP (show APRT Proteins) formation
sphingosylphosphorylcholine and lysophosphatidic acid are not the ligands for GPR4 and that this receptor may constitutively inhibit ERK1/2 activation
Collectively, these results posit the acid sensor GPR4 as a novel component of central blood pressure control through interactions with the renin (show REN Proteins)-angiotensin system.
knockdown of a proton-sensing G protein-coupled receptor (show GPR34 Proteins) GPR4 markedly reduced CHOP (show DDIT3 Proteins) expression and endothelial cell apoptosis after hypoxia exposure.
The results indicate that through the G12 (show TCF3 Proteins)/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 Proteins) 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 Proteins) 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 Proteins) 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