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

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

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

2. 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.

3. S1PR1 (show S1PR1 ELISA Kits)/3 silencing alters proliferation, adhesion, viability and lateral motility in estrogen receptor (show ESR1 ELISA Kits)-negative MCF-7 and estrogen receptor (show ESR1 ELISA Kits)-positive MDA-MB-231 breast cancer cells.

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

5. The S1P1,3 activation results in Akt (show AKT1 ELISA Kits) phosphorylation and subsequent activation of eNOS (show NOS3 ELISA Kits) via phosphorylation at serine(1177) and dephosphorylation at threonine(495).

6. HDL (show HSD11B1 ELISA Kits)-associated ApoM (show APOM ELISA Kits) is anti-apoptotic by delivering sphingosine 1-phosphate to S1P1 (show S1PR1 ELISA Kits) and S1P3 receptors on vascular endothelium.

7. The study shows that S1P receptor 3 (S1PR3) mRNA is overexpressed in EBV-positive NPC (show NPC1 ELISA Kits) patient-derived xenografts and a subset of primary NPC (show NPC1 ELISA Kits) tissues, and that knockdown of S1PR3 suppressed the activation of AKT (show AKT1 ELISA Kits) and the S1P-induced migration of NPC (show NPC1 ELISA Kits) cells.

8. S1pr3 promotes leukocyte rolling by mobilization of endothelial P-selectin (show SELP ELISA Kits).

9. Stimulation with sphingosine-1-phosphate enhances cancer stem cells via S1PR3 and subsequent Notch1 (show NOTCH1 ELISA Kits) activation.

10. TRPC1 (show TRPC1 ELISA Kits) functions as a major regulator of S1P3 and VEGFR2 (show KDR ELISA Kits) expression.

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

1. 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.

2. The findings of this study demonstrated that S1P3 and Sphk1 (show SPHK1 ELISA Kits) are mediators of inflammatory signaling and are upregulated in astrocytes in response to injury.

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

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

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

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

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

8. The role of the S1PR3/PDGFR-beta (show PDGFRB ELISA Kits)/Akt (show AKT1 ELISA Kits) pathway in sphingosine-1-phosphate -induced endothelial progenitor cells migration and angiogenesis

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

10. Smad3 (show SMAD3 ELISA Kits) deficiency leads to mandibular condyle degradation via the sphingosine 1-phosphate (S1P (show S1PR1 ELISA Kits))/S1P3 signaling axis