- Table of Contents
We validate the specificity of these antibodies to S1PR3 by testing them on tissues known to express S1PR3 positively and negatively. Browse below to find the S1PR3 antibody that suites your experiment. We have 4 of these antibodies and many publications and validation images.
If you cannot find antibodies that fit your needs, contact us for making custom antibodies. We have a full suite of custom antibody services covering from research to diagnostic and therapeutic applications.
Facts about Sphingosine 1-phosphate receptor 3.
When expressed in rat HTC4 hepatoma cells, is capable of mediating S1P-induced cell proliferation and suppression of apoptosis. .
|G-protein coupled receptor 1 family|
EDG3; EDG-3; EDG3FLJ37523; Endothelial differentiation G-protein coupled receptor 3; endothelial differentiation, sphingolipid G-protein-coupled receptor, 3; FLJ93220; G protein-coupled receptor, endothelial differentiation gene-3; LPB3; MGC71696; S1P receptor 3; S1P receptor EDG3; S1P receptor Edg-3; S1P3; S1PR3; sphingosine 1-phosphate receptor 3; Sphingosine 1-phosphate receptor Edg-3; sphingosine-1-phosphate receptor 3
|Sequence:||9; NC_000009.12 (88991468..89005155)|
Expressed in all tissues, but most abundantly in heart, placenta, kidney, and liver.
Cell membrane; Multi-pass membrane protein.
S1PR3 is a marker that is used in the diagnosis of cerebral ischemia. There are various drugs that act as S1PR3 modulators for the treatment of MS. This article will discuss the advantages of using S1PR3 to detect cerebral ischemia. This article also discusses the effects of chronic drug exposure on S1PR3.
It is not clear what S1P3 does in cerebral ischemia. S1P3 is linked to the inflammatory response associated M1 polarization activated microglia. These data suggest that S1P3 may be a new mediator of brain injury caused by tMCAO. This study may help us identify the best treatment for such a condition.
Researchers have shown S1P3 function as a predictor or indicator of cerebral ischemia. S1P3 is thought to play a cardioprotective function in mice that have been shown to increase the severity of myocardial damage by deleting S1P2 and S1PR3. It also reduces tissue injury and increases expression anti-inflammatory cytokines.
In a mouse model of cerebral ischemia, S1PR3 was inhibited by the S1P receptor inhibitor CAY10444. Researchers used western blotting and immunofluorescence to determine changes in S1PR3 gene expression after cerebral injury. This finding provides a new way to detect and monitor cerebral ischemia in the early stages of the disease.
The S1P receptor is a novel pathwayogenic protein in cerebral ischemia. It has also been identified as a crucial factor in microglial activation. S1P receptors can negatively affect the heart so they are not considered therapeutic targets. An antagonist could be a more effective treatment strategy for cerebral ischemia. There are several inflammatory responses that the brain may experience from the S1P subtypes.
S1P3 regulates activated microglia's M1 Polarization in the brain. This activates NF-kB's signaling system. It also affects the phosphorylation and activation of downstream effector pathway in ischemic brain. S1P3 may be a new marker for cerebral ischemia. However it is still a key indicator and predictor.
It is not clear what role S1P3 plays in focal cerebral ischemia. However, studies have shown that inhibiting S1P2 activity, FTY720-phosphate, and TY-52156, a specific S1P3 antagonist, can prevent the onset of cerebral ischemia and improve cerebral hemorrhage. Studies in mice lacking S1P3 receptors have confirmed these findings.
Multiple S1PR3-based modulators are approved or in development. The current generation S1PR modators is very specific for S1PR1; it is expected that it will decrease bradycardia, as well other cardiovascular risk factors. Further studies are needed to determine if selective S1PR modulators work in MS patients. Although fingolimod has been approved since 2003, the second-generation S1PR moduleator is expected be more effective and to have fewer side effects.
There are currently four S1PR3 inhibitors approved or in development. These drugs target S1P and regulate the regulation of circulating lymphocytes. Multiple Sclerosis (MS), IBD (inflammatory bowel disease) and IBS (inflammatory bowel disease) share a common dysregulation. Consequently, S1PR modulators may help treat other conditions affecting the immune system.
Fingolimod is the most effective S1PR3 inhibitor, while ozanimod is the least effective. Ozanimod decreases the absolute lymphocyte count by inhibiting lymphocyte egress through lymph nodes. These compounds may be beneficial for MS even though there aren't any studies that can confirm their efficacy.
Although several S1PR3 modulators have been approved for MS, their application in other inflammatory conditions is now possible. Ozanimod, for example, is being evaluated for Crohn’s Disease and Ulcerative Colitis and is currently in phase 3 clinical trials for MS. Although this treatment is promising for MS sufferers, further trials are necessary to verify its effectiveness. Furthermore, researchers will need to identify biomarkers for the therapy in patients.
Other S1PR3 inhibitors are siponimod, ceralifimod, ozanimod and siponimod. These drugs are not able modulate S1PR2, but they are highly selective for S1PR3. This means that although fingolimod has been approved for MS treatment, it is not yet available for this indication.
Fingolimod (a combination of Merck Pharmaceuticals and Ono Pharmaceuticals) is a possible candidate for MS treatment. It reduces the number of GdE lesions on monthly scans over 26 weeks. It reduced GdE lesion count by as much as 82% and extended the study duration by 7 days. Due to changes in MS disease-modifying therapies, the extension study had to be terminated.
S1PR3 Modulators are known to inhibit ROCK Activity, which is essential for S1P-induced activation YAP. This inhibition was observed after treating ASMCs either with S1P alone, or with Y27632. Inhibitors also inhibited S1P induced ASMC proliferation, migration and contraction.
In addition to the ability to inhibit inflammatory cytokines, S1P is involved in multiple cellular processes, including immune response and vascular barrier integrity. The development of novel therapies targeting S1P signaling is advancing, with several S1PR modulators currently in development for ulcerative colitis and Crohn's disease. Patients with IBD will find the new agents in S1P signaling a safe and practical strategy.
In this study, we investigated the effect of S1P in ASMC migration as well as collagen gel contraction. S1P treatment led to ASMC migration being promoted over that of the control group. 0.3% Methanol had no effect. The S1P-induced significant contraction in collagen gel, according the authors. The researchers concluded that S1P induces antagonism with chronic exposure to drug.
S1P significantly elevated FOXM1 & cyclinD1 protein levels in comparison to the control. However, S1P-induced FOXM1 and cyclin D1 expression were reduced by JTE013 and CAY10444. This suggests that S1P-induced FOXM1 expression is upregulated at higher levels by FOXM1 protein and S1PR2.