Sphingosine-1-Phosphate Receptor 3 (S1PR3) ELISA Kits

Human Sphingosine-1-Phosphate Receptor 3 (S1PR3) interaction partners

1. these findings argue that HDL promotes angiogenesis via S1P3-dependent up-regulation and activation of VEGFR2 and also suggest that the S1P-S1P3-VEGFR2 signaling cascades as a novel target for HDL-modulating therapy implicated in vascular remodeling

2. S1P induced the expression of some asthma-related genes, such as ADRB2, PTGER4, and CCL20, in bronchial epithelial cells. The knock-down of SIPR3 suppressed the expression of S1P-inducing CCL20.

3. Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.

4. Authors found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway.

5. Sphingosine-1-phosphate receptor 3 (S1PR3) mediates multiple aspects of the inflammatory response during sepsis.

6. in breast cancer cells overexpression of S1P3 and its activation by S1P has pro-inflammatory and pro-metastatic potential by inducing COX-2 expression and PGE2 signaling via EP2 and EP4.

7. S1PR1/3 silencing alters proliferation, adhesion, viability and lateral motility in estrogen receptor-negative MCF-7 and estrogen receptor-positive MDA-MB-231 breast cancer cells.

8. High S1PR3 expression is associated with increased lung adenocarcinoma.

9. The S1P1,3 activation results in Akt phosphorylation and subsequent activation of eNOS via phosphorylation at serine(1177) and dephosphorylation at threonine(495).

10. HDL-associated ApoM is anti-apoptotic by delivering sphingosine 1-phosphate to S1P1 and S1P3 receptors on vascular endothelium.

11. The study shows that S1P receptor 3 (S1PR3) mRNA is overexpressed in EBV-positive NPC patient-derived xenografts and a subset of primary NPC tissues, and that knockdown of S1PR3 suppressed the activation of AKT and the S1P-induced migration of NPC cells.

12. S1pr3 promotes leukocyte rolling by mobilization of endothelial P-selectin.

13. Stimulation with sphingosine-1-phosphate enhances cancer stem cells via S1PR3 and subsequent Notch1 activation.

14. TRPC1 functions as a major regulator of S1P3 and VEGFR2 expression.

15. Data show that sphingosine kinase SphK1 and sphingosine-1-phosphate (S1P) receptors S1P1, S1P2, S1P3, and S1P5 were expressed from primary, up to recurrent and secondary glioblastomas, with sphingosine kinase SphK2 levels were highest in primary tumors.

16. Data indicate that sphingosine 1-phosphate (S1P) and hepatocyte growth factor (HGF) induced transloaction of integrin beta4, S1P receptors S1PR2 and S1PR3 to endothelial cell membrane caveolin-enriched microdomains (CEMs).

17. we provide evidences that S1PR1/3, but not S1PR2, negatively regulate the expression of collagen in hMSCs using cellular and molecular approaches in vitro

18. key role of Sphk1, S1PR1 and S1PR3 in angiogenesis underlying the liver fibrosis process

19. a novel signaling axis, i.e., ROCK-JNK-ETS-1-CD44 pathway, which plays an essential role in the S1P3-regulated chemotactic response.

20. associations were found for 2 promoter SNPs across 2 European descent samples supporting association of alleles -1899G and -1785C with decreased risk for sepsis-associated acute respiratory distress syndrome (ARDS); alleles reduced transcription factor binding to S1PR3 promoter and S1PR3 promoter activity; associated with lower plasma S1PR3 protein in ARDS patients

Mouse (Murine) Sphingosine-1-Phosphate Receptor 3 (S1PR3) interaction partners

1. the proinflammatory lipid sphingosine 1-phosphate (S1P) and its receptor, S1P receptor 3 (S1PR3), trigger itch and pain behaviors via distinct molecular and cellular mechanisms.

2. This study identified S1P3 as a pathogenic mediator in an ischemic brain along with underlying mechanisms, involving its modulation of microglial activation and M1 polarization.

3. Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.

4. There is considerable sexual dimorphism in the vascular and metabolic responses of aged mice and that reduced signaling through S1PR3 could be one mechanism to explain these effects.

5. The findings of this study demonstrated that S1P3 and Sphk1 are mediators of inflammatory signaling and are upregulated in astrocytes in response to injury.

6. Sphingosine-1-phosphate receptor 3 (S1PR3) mediates multiple aspects of the inflammatory response during sepsis.

7. The absence of S1P3 appears responsible for a lower availability of calcium during fatigue.

8. These results highlight an important role for S1PR3 in Hematopoietic stem and progenitor cell niche occupancy.

9. S1P3 deletion protects mouse soleus from age-related drop in muscle mass, force, and regenerative capacity.

10. The finding that S1P3 receptor- and Galpha13-mediated RhoA activation is responsible for protection against ischemia/reperfusion suggests that selective targeting of S1P3 receptors could provide therapeutic benefits in ischemic heart disease.

11. The role of the S1PR3/PDGFR-beta/Akt pathway in sphingosine-1-phosphate -induced endothelial progenitor cells migration and angiogenesis

12. P2RY8 promotes clustering of activated B cells within follicles in a follicular dendritic cell (FDC)-dependent manner.

13. Smad3 deficiency leads to mandibular condyle degradation via the sphingosine 1-phosphate (S1P)/S1P3 signaling axis

14. S1pr3 promotes leukocyte rolling by mobilization of endothelial P-selectin.

15. The role of sphingosine-1-phosphate in the production of immature double-negative thymocytes in experimental and chronic Chagas disease is reported.

16. CTGF exerts profibrotic action in myoblasts via the up-regulation of sphingosine kinase-1/S1P3 signaling axis in TGF-beta dependent manner.

17. results indicate that S1P3 receptor signaling plays an important role in pulmonary inflammation and fibrosis and that this signaling occurs via CTGF expression

18. key role of Sphk1, S1PR1 and S1PR3 in angiogenesis underlying the liver fibrosis process

19. Data show that two S1P receptors, S1P2 and S1P3, are collectively essential mediators of eyelid closure during murine development.

20. signalling though S1PR3 suppresses cell cycle progression to regulate function in muscle satellite cells