https://pubmed.ncbi.nlm.nih.gov/33410533/
S1P3 plays an essential role in the pathophysiological processes related to inflammation, cell proliferation, cell migration, tumor invasion and metastasis, ischemia-reperfusion, tissue fibrosis, and vascular tone. In this paper, the relevant mechanism in the role of S1P3 is summarized. Keywords: S1P3; function; sphingosine 1‐phosphate.

https://en.wikipedia.org/wiki/S1PR3
S1PR3. Sphingosine-1-phosphate receptor 3 also known as S1PR3 is a human gene which encodes a G protein-coupled receptor which binds the lipid signaling molecule sphingosine 1-phosphate (S1P). Hence this receptor is also known as S1P3.

https://www.nature.com/articles/s41467-018-05030-w
S1P3 mediates its effects on BTB permeability through astrocytic secretion of IL-6 and CCL2, which relaxes endothelial cell adhesion. Tumor cell overexpression of S1P3 mimics this pathway

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265592/
1.1. Mechanism of Action of S1P/S1PR. The cell membrane is composed of a large number of proteins, among them sphingosines, which in turn are the source of many bioactive lipids, including ceramide, sphingosine, S1P and ceramide-1-phosphate [7,8].S1P is the active terminal derivative of sphingosine metabolism, generated by the action of sphingosine kinase (SKs) [9,10].

https://www.nature.com/articles/s41422-021-00567-w
Cell Research - Structural insights into sphingosine-1-phosphate recognition and ligand selectivity of S1PR3-Gi signaling complexes

https://onlinelibrary.wiley.com/doi/10.1002/jcp.29958
S1P1, S1P2, and S1P3 are extensively expressed in a wide variety of different tissues. The expression of S1P4 is restricted to lymphoid and hematopoietic tissues, while S1P5 is primarily expressed in the nervous system. S1P3 plays an essential role in the pathophysiological processes related to inflammation, cell proliferation, cell migration

https://www.science.org/doi/10.1126/sciadv.abf5325
Sphingosine-1-phosphate (S1P) is a lysophospholipid characterized by a single alkyl chain and was initially identified as a phospholipid precursor and metabolite ().S1P is a signaling molecule that acts through five GPCRs (S1PR1 to S1PR5) (15-17), among which S1PR3 couples to G q/11, G i/o, and G 12/13 upon S1P binding and regulates immune responses including P-selectin-dependent leukocyte

https://www.nature.com/articles/s41422-021-00566-x
Lipid signaling has long been recognized as a critical regulator of cellular processes. Sphingosine-1-phosphate (S1P), a metabolic product of cell membrane sphingolipids, is a ubiquitous

https://www.ncbi.nlm.nih.gov/gene/1903
TRPC1 functions as a major regulator of S1P3 and VEGFR2 expression. 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.

https://pubmed.ncbi.nlm.nih.gov/19282351/
The S1P3 receptor, while expressed at lower levels, mediates the bradycardic effect of S1P agonists. Studies using knockout mice indicate that S1P2 and S1P3 receptors play a major role in mediating cardioprotection from ischaemia/reperfusion injury in vivo. S1P receptors are also involved in remodelling, proliferation, and differentiation of

https://www.sciencedirect.com/science/article/pii/S0009898121001108
Sphingosine-1-phosphate (S1P) is a bioactive lipid which regulates a series of physiological and pathological processes via binding to five S1P receptors (S1PR1-5). Although S1PR1-3 are widely expressed, the study of S1PRs, however, mainly addressed S1PR1 and S1PR2, and few studies focus on S1PR3-5. In recent years, a growing number of studies

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072483/
Indeed, S1P1 and S1P3 signal migratory responses and amplify those exerted by other growth factors, whereas S1P2 signals inhibition of growth factor-evoked migration [185,197]. The possible reason of this antagonistic effect appears to reside in the fact that S1P1 and S1P3 stimulate the small GTPase Rac, whereas S1P2 inhibits it .

https://www.frontiersin.org/articles/10.3389/fnmol.2017.00317/full
Depletion of S1P3 receptors however resulted in a dramatic inhibition of S1P-induced neurite retraction and was on the contrary associated with a significant elongation of neuronal processes in response to S1P. Opposing responses to S1P could be observed in the same neuron population, where S1P could activate S1P1 receptors to stimulate

https://www.genecards.org/cgi-bin/carddisp.pl?gene=S1PR3
S1PR3 (Sphingosine-1-Phosphate Receptor 3) is a Protein Coding gene. Diseases associated with S1PR3 include Dermatitis, Atopic, 7 and Pulmonary Edema.Among its related pathways are GPCR downstream signalling and ESR-mediated signaling.Gene Ontology (GO) annotations related to this gene include G protein-coupled receptor activity and integrin binding.

https://www.jbc.org/article/S0021-9258(19)71187-9/fulltext
In the targeted S1P3 ES cell line, the wild-type S1P3 allele and the recombined S1P3 allele were identified as 13-kb and 3-kb bands, respectively, on Southern blots (Fig. 1D, top). These targeted ES cell lines were used to produce chimeric mice that transmitted the targeted alleles to their offspring, resulting in heterozygous mice.

https://www.nature.com/articles/s41467-019-10904-8
S1PR3 is a G protein coupled receptor, that has a role in inflammation. Here the authors show that in the CNS, S1PR3 may contribute to resilience to stressful experiences; resilient rodents show

https://pubmed.ncbi.nlm.nih.gov/30917625/
In this study, the roles of S1P 3 on inflammatory response were investigated in primary peritoneal macrophages. S1P 3 receptor was induced along with sphingosine kinase 1 by stimulation of lipopolysaccharide (LPS). LPS treatment induced inflammatory genes, such iNOS, COX-2, IL-1β, IL-6 and TNF-α. TY52156, an antagonist of S1P 3 suppressed the

https://www.sciencedirect.com/science/article/abs/pii/S0009898121001108
Sphingosine-1-phosphate (S1P) is a bioactive lipid which regulates a series of physiological and pathological processes via binding to five S1P receptors (S1PR1-5). Although S1PR1-3 are widely expressed, the study of S1PRs, however, mainly addressed S1PR1 and S1PR2, and few studies focus on S1PR3-5. In recent years, a growing number of studies

https://www.nature.com/articles/s41374-020-00505-1
The role of sphingosine kinase isoforms and receptors S1P1,S1P2,S1P3,and S1P5 in primary,secondary,and recurrent glioblastomas. Tumor Biol. 2014;35:8979-89. CAS Google Scholar

https://pubmed.ncbi.nlm.nih.gov/34445567/
Abstract. S1P is the final product of sphingolipid metabolism, which interacts with five widely expressed GPCRs (S1P 1-5 ). Increasing numbers of studies have indicated the importance of S1P 3 in various pathophysiological processes. Recently, we have identified a pepducin (compound KRX-725-II) acting as an S1P 3 receptor antagonist.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4702096/
Schürer SC, Brown SJ, Gonzalez-Cabrera PJ, Schaeffer MT, Chapman J, Jo E, Chase P, Spicer T, Hodder P, Rosen H. (2008) Ligand-binding pocket shape differences between sphingosine 1-phosphate (S1P) receptors S1P1 and S1P3 determine efficiency of chemical probe identification by ultrahigh-throughput screening. ACS Chem Biol 3:486-498.

https://pubmed.ncbi.nlm.nih.gov/26494861/
The molecular pharmacology of the G protein-coupled receptors for sphingosine 1-phosphate (S1P) provides important insight into established and new therapeutic targets. A new, potent bitopic S1P3 antagonist, SPM-354, with in vivo activity, has been used, together with S1P3-knockin and S1P3-knockout

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2924669/
S1P3 deficient and sufficient immature B cells egress from bone marrow with similar kinetics. Non-autoreactive immature B cells use S1P3 to migrate to S1P in vitro, thus we questioned whether S1P3 responding to S1P might contribute to immature B cell exit from bone marrow.