mProX™ Human S1PR1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Elevating S1PR1 levels within HAECs enhances the proliferation potential of hepatocellular carcinoma (HCC) cells.
CCK-8 experiments were conducted to assess the viability of hepatocellular carcinoma (HCC) cell lines (Huh7 and SK-Hep1) when co-cultured with endothelial cells (ECs) exhibiting S1PR1 gene knockdown.
Ref: Wang, Xuehong, et al. "S1PR1 induces metabolic reprogramming of ceramide in vascular endothelial cells, affecting hepatocellular carcinoma angiogenesis and progression." Cell Death & Disease 13.9 (2022): 768.
Pubmed: 36068200
DOI: 10.1038/s41419-022-05210-z
Research Highlights
Wunsch F, et al. "Structural determinants of sphingosine-1-phosphate receptor selectivity.." Archiv der Pharmazie, 2023.
In this study, the researchers focused on the drug fingolimod, which is the prodrug of fingolimod-1-phosphate (F1P) that was the first approved sphingosine-1-phosphate receptor (S1PR) modulator for treating multiple sclerosis. F1P targets all five S1PR subtypes, including S1PR(1) and S1PR(3). While S1PR(1) activation is linked to immune modulatory effects, S1PR(3) activation can cause cardiac adverse effects. To address this, the researchers used a combination of molecular dynamics simulations and three-dimensional pharmacophores (dynophores) to investigate the binding site characteristics of specific S1PR subtypes. This research has potential implications for the development of new drugs targeting S1PR subtypes, such as ozanimod and siponimod, as well as pharmaceutical tool compounds like CYM5541.
Pubmed:
37806764
DOI:
10.1002/ardp.202300387
Skoug C, et al. "Density of Sphingosine-1-Phosphate Receptors Is Altered in Cortical ." Neurochemical research, 2023.
Sphingosine-1-phosphate (S1P), a phosphosphingolipid, has diverse biological functions. It acts as an intracellular second messenger and as an extracellular ligand to five G-protein coupled receptors (S1PR1-5). In the brain, S1P plays a crucial role in regulating neuronal proliferation, apoptosis, synaptic activity, and neuroglia activation. Recently, altered S1P metabolism has been observed in neurodegenerative disorders. Previous research has demonstrated the presence of S1PRs in nerve terminals, exhibiting distinct sub-synaptic localization and neuromodulation actions. Given that synaptic dysfunction is associated with conditions such as type 2 diabetes (T2D), the researchers hypothesized that S1P signaling may be modified in nerve terminals. The current study aimed to determine the density of S1PRs in cortical synaptosomes in insulin-resistant Goto-Kakizaki (GK) rats and Wistar control rats, as well as in mice fed a high-fat diet (HFD) and low-fat-fed controls. The results revealed that, compared to their respective control groups, GK rats had similar cortical S1P levels despite having higher plasma levels. However, they had a lower density of S1PR1, S1PR2, and S1PR4 in nerve-terminal-enriched membranes. Similarly, HFD-fed mice showed increased plasma and cortical S1P concentrations and a decreased density of S1PR1 and S1PR4. These findings suggest that there may be altered S1P signaling in synapses of models with insulin resistance and diet-induced obesity, potentially implicating S1P signaling in T2D-associated synaptic dysfunction.
Pubmed:
37794263
DOI:
10.1007/s11064-023-04033-4