S1PR1

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S1PR1

A gene on chromosome 1p21 that encodes an EDG (endothelial differentiation, G protein-coupled) family receptor, which is highly expressed in endothelial cells. It binds the sphingosine-1-phosphate with high affinity and high specificity, and may be involved in regulating endothelial cell differentiation. Receptor activation induces cell–cell adhesion.
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Ponesimod is a selective sphingosine-1-phosphate receptor 1 (S1P1) modulator, a class of drugs that is believed to functionally inhibit S1P activity and reduce the number of circulating lymphocytes by trapping them in the lymph nodes.
Mayzent selectively binds to S1P1 and S1P5 receptors.
Celgene announced additional phase III data analyses evaluating the efficacy and safety of ozanimod, a novel, oral, selective sphingosine 1-phosphate 1, or S1P1, and 5, or S1P5, receptor modulator, versus interferon beta-1a in patients with relapsing multiple sclerosis, or RMS.
Singh, "Quantitative structure-activity relationship study of substituted-[1, 2, 4] oxadiazoles as s1p1 agonists," Journal of Current Chemical and Pharmaceutical Sciences, vol.
Moreover, sphingolipid metabolites, such sphingosine1phosphate (S1P), promote the switching phenotype of mouse macrophages from M1- to M2-like state, by activating S1P1 receptor [208].
Gonzalez-Cabrera et al., "Enhancement of capillary leakage and restoration of lymphocyte egress by a chiral S1P1 antagonist in vivo," Nature Chemical Biology, vol.
The pathophysiology underlying fingolimod-associated macular oedema is conjectured to be a consequence of perturbation of the blood-retinal barrier since S1P1 and S1P3 receptors have a pivotal role in regulating the function of the endothelial and epithelial barriers.49 Patients with pre-existing diabetes were excluded from the fingolimod trials in patients with MS owing to the data received from patients receiving the drug who had undergone a renal transplant as alluded to earlier.
The researchers determined that a particular gene, S1P1, is vital for the proper formation of the heart.
First, S1P1 transcripts are also abundant in the ECs and vascular smooth muscle cells surrounding blood vessels, and strong [S1P.sub.1] activation is detected in both the lymphatic and vascular ECs in lymphoid tissues, where most lymphocytes show no evidence of [S1P.sub.1] activation under homeostatic conditions.
Michel, "VEGF induces S1P1 receptors in endothelial cells: Implications for cross-talk between sphingolipid and growth factor receptors," Proceedings of the National Academy of Sciences of the United States of America, vol.