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CONCLUSION: MiR (zeige MLXIP Proteine)-126 down-regulated S1PR2 and then prevented the activation of PI3K (zeige PIK3CA Proteine)/AKT (zeige AKT1 Proteine) signaling pathway, which ultimately could damage intestinal mucosal barrier function.
Data suggest that activation of SR-BI (zeige SCARB1 Proteine) by APOAI down-regulates sphingosine 1-phosphate/S1PR2-mediated inflammation in vascular endothelial cells by activating the PI3K (zeige PIK3CA Proteine)/Akt (zeige AKT1 Proteine) signaling pathway; oxidized-LDL does the opposite. (APOA1 (zeige APOA1 Proteine) = apolipoprotein A-I (zeige APOA1 Proteine); SR-BI/SCARB1 (zeige SCARB1 Proteine) = scavenger receptor class B type I; S1PR2 = sphingosine 1-phosphate receptor 2; PI3K (zeige PIK3CA Proteine) = phosphatidylinositol 3-kinase; Akt (zeige AKT1 Proteine) = proto-oncogene c-akt (zeige AKT1 Proteine))
S1PR2 mediates Rho activation in normal cells neighboring RasV12-transformed cells.
Sphingosine 1-phosphate-induced IL-8 (zeige IL8 Proteine) gene expression is mainly regulated via S1PR(1 (zeige S1PR1 Proteine)), and its secretion is regulated through S1PR(2) receptor subtype.
S1PR2 is repressed by FOXP1 (zeige FOXP1 Proteine) in activated B-cell and germinal center B-cell DLBCL cell lines with aberrantly high FOXP1 (zeige FOXP1 Proteine) levels; S1PR2 expression is further inversely correlated with FOXP1 (zeige FOXP1 Proteine) expression in 3 DLBCL patient cohorts.
LXR-alpha (zeige NR1H3 Proteine) might downregulate S1PR2 expression via miR (zeige MLXIP Proteine)-130a-3p in quiescent HUVECs. Stimulation of TNF-alpha (zeige TNF Proteine) attenuates the activity of LXR-alpha (zeige NR1H3 Proteine) and results in enhanced S1PR2 expression.
S1PR2 plays a critical role in TCA-induced COX-2 expression and CCA (zeige FBN2 Proteine) growth and may represent a novel therapeutic target for CCA (zeige FBN2 Proteine).
both S1PR1 (zeige S1PR1 Proteine) and S1PR2 play a pivotal role in hyperglycemia-induced EC dysfunction and endothelial injury by reducing and enhancing the production of oxidative stress.
AB1 displayed potency at least equivalent to JTE-013 in affecting signaling molecules downstream of S1P2.
Activation of S1PR2-calcium influx-RhoA (zeige RHOA Proteine)/ROCK dominates the high-dose S1P (zeige MBTPS1 Proteine)-induced endothelial monolayer hyperpermeability response.
Results provide evidence that S1PR2 plays an essential role in modulating proinflammatory cytokine production and osteoclastogenesis.
activation of S1P2 with a selective receptor agonist increases cell viability and reduces cisplatin-mediated cell death by reducing ROS (zeige ROS1 Proteine). Cumulatively, these results suggest that S1P2 may serve as a therapeutic target for attenuating cisplatin-mediated ototoxicity.
S1P2 receptor is a key signaling molecule in the S1Pdependent inhibition of adipogenic differentiation.
S1PR2, as a critical receptor in macrophages, impairs phagocytosis and antimicrobial defense in the pathogenesis of sepsis.
These results suggest that S1PR2 and CXCR5 (zeige CXCR5 Proteine) cooperatively regulate localization of Tfh cells in GCs (zeige UGCG Proteine) to support GC responses
The sphingolipid receptor S1PR2 is a receptor for Nogo-a (zeige RTN4 Proteine) repressing synaptic plasticity.
S1PR2 expression was increased in disease-susceptible regions of the CNS of female SJL EAE mice compared with their male counterparts.
IL-6 (zeige IL6 Proteine) increased the number of osteoclast precursor cells in tibial bone marrow via up-regulating S1PR2, thus playing a crucial role in systemic bone loss induced by inflammation.
Sphingosine-1-phosphate receptor 2 protects against anaphylactic shock through suppression of endothelial nitric oxide synthase (zeige NOS3 Proteine) in mice.
Data show that two S1P (zeige S1PR1 Proteine) receptors, S1P2 and S1P3 (zeige S1PR3 Proteine), are collectively essential mediators of eyelid closure during murine development.
This gene encodes a member of the G protein-coupled receptors, as well as the EDG family of proteins. This protein participates in sphingosine 1-phosphate-induced cell proliferation, survival, and transcriptional activation
sphingosine-1-phosphate receptor 2
, sphingosine 1-phosphate receptor 2-like
, S1P receptor 2
, S1P receptor EDG5
, S1P receptor Edg-5
, endothelial differentiation G-protein coupled receptor 5
, endothelial differentiation, sphingolipid G-protein-coupled receptor, 5
, sphingosine 1-phosphate receptor 2
, sphingosine 1-phosphate receptor Edg-5
, G-protein coupled receptor 13
, lysophospholipid receptor B2
, sphingosine-1-phosphate receptor S1P(2)
, G-protein coupled receptor H218