S1PR1

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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Western blotting was used to detect apoptosis-related proteins, expression of S1PR1, and the phosphorylation status of STAT3.
It is an oral and selective sphingosine 1-phosphate 1 (S1PR1) and 5 (S1PR5) receptor modulator in development for immune-inflammatory indications such as ulcerative colitis and Crohn's disease, in addition to multiple sclerosis.
The therapeutic options related to S1P/S1PR signalling are numerous as demonstrated by several clinical trials [31] and the recent approval by the Food and Drug Administration and the European Medicines Agency of FTY720 (Fingolimod, Gilenya, Novartis) for the treatment of relapsing multiple sclerosis [43, 44], acting as functional S1PR1 antagonist [45].
As a miRNA, miRNA-542-3p plays the role of tumor suppressor in a variety of malignant tumors, such as posttranscriptional regulation of BIRC5 in bladder cancer [17], targeting the AKT pathway in human astrocytoma [18], targeting the oncogene metadherin in gastric cancer [19], and interfering with S1PR1 in breast cancer [20].
One of the most important breakthroughs in this field was the discovery of the role of sphingosine-1 phosphate (S1P) which acts via its receptors S1PR1 and S1PR2 present on monocytes, as a vital regulator of monocyte bone homing in mice.
A multitude of the immunomodulatory effects of S1P have been attributed to signaling through S1PR1, whereas the contribution of other S1P receptors remains largely obscure.
S1pr1 and Cd69 genes were downregulated in AIRmax mice and were predicted targets of miR-106a-5p, miR-25-3p, and miR-20b-5p.
The failure of these cells to exit the tissue is currently thought to be due to their low expression of the transcription factor KLF2 and of S1PR1 and to their high expression of the C-type lectin CD69; as a result of these conditions, the cells fail to respond to an "exit cue" provided by S1P (sphingosine-1-phosphate), which is released mainly from lymphatic ECs.
In immature neurons, the activation of S1PR1 activates neurite outgrowth whereas S1PR2 or S1PR5 exerts inhibitory effects in vitro [28].
Fingolimod modulates the activity of sphingosine-1phosphate receptors (S1PR1), thereby inhibiting T lymphocyte migration from the central nervous system [42] lymph nodes, and thus acts on the first step of MS--neuroinflammatory.
This reduction of B cells in the blood occurs following an impaired splenocyte response to S1P by downregulating S1PR1 expression on splenocytes [55].
Thus, genomic studies on marbling have been performed to discover marbling-specific genes including ribosomal protein L27a (RPL27A), sphingosine-1-phosphate receptor 1 (S1PR1), ADAM metallopeptidase with thrombospondin type 1 motif 4 (ADAMTS4), hormone-sensitive lipase (LIPE), peroxisome proliferator-activated receptor alpha (PPAR), CCAAT/enhancer binding protein (C/EBP), alpha (CEBPA), runt-related transcription factor 1 (RUNX1), and insulin (INS) in animal breeding researches (Lee et al., 2008).