mProX™ Human S1PR3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 In vitro, the S1P/S1PR3 signaling pathway promotes the proliferation of osteosarcoma (OS) cells.
Suppression of S1PR3 resulted in diminished proliferation of osteosarcoma (OS) cells, MNNG-HOS, and U-2OS, as evidenced by colony formation assays. The left panel displays representative images of these colonies (scale bars = 5 mm). Significance levels: **p < .01, ***p < .001, determined by Student's t-test.
Ref: Shen, Yifei, et al. "S1P/S1PR3 axis promotes aerobic glycolysis by YAP/c-MYC/PGAM1 axis in osteosarcoma." EBioMedicine 40 (2019): 210-223.
Pubmed: 30587459
DOI: 10.1016/j.ebiom.2018.12.038
Research Highlights
Wunsch F, et al. "Structural determinants of sphingosine-1-phosphate receptor selectivity.." Archiv der Pharmazie, 2023.
The prodrug Fingolimod, approved for the treatment of multiple sclerosis, was the first to target all five subtypes of the sphingosine-1-phosphate receptor (S1PR) through its active form, fingolimod-1-phosphate (F1P). However, while agonism at the S1PR(1) subtype leads to desired immune modulatory effects, agonism at S1PR(3) is associated with cardiac adverse effects. To address this issue, second generation S1PR(1,5) selective ligands like siponimod and ozanimod were developed. Using a combination of molecular dynamics simulations and three-dimensional pharmacophores (dynophores), the binding site characteristics and subtle differences in receptor-ligand interactions of each subtype were investigated. This study provides insights into the selectivity profile of approved drugs like ozanimod and siponimod, as well as pharmaceutical tool compounds like CYM5541, contributing to a better understanding of their mechanism of action.
Pubmed:
37806764
DOI:
10.1002/ardp.202300387
Wagner JM, et al. "Pharmacological elevation of sphingosine-1-phosphate by S1P lyase inhibition ." Journal of cellular and molecular medicine, 2023.
Posttraumatic osteomyelitis is a debilitating complication that occurs after open fractures and often leads to bone defects. Currently, there are limited treatment options available for this condition. However, recent studies have identified the potential for S1P signaling to have osteoanabolic effects. To further investigate this, researchers tested the effects of raising S1P levels using the drug DOP in a mouse model of posttraumatic osteomyelitis. They also studied the effects of S1PR3 deficiency on bone regeneration and confirmed the potential for S1P/S1PR3 signaling to be a promising target for therapeutic intervention in human bone samples. Results showed that DOP treatment significantly enhanced bone growth and improved osteoblastogenesis and angiogenesis in both the mouse model and human bone samples. This highlights the potential of targeting S1P/S1PR3 signaling in promoting bone regeneration in posttraumatic osteomyelitis.
Pubmed:
37710406
DOI:
10.1111/jcmm.17952
