Sphingosine 1-Phosphate ELISA Kit

Name: Sphingosine 1-Phosphate ELISA Kit
SKU: DEIA-XYZ5
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

blood, serum, synovial fluid, cell lysate, tissue lysate

Species Reactivity

Human

Intended Use

The S1P-ELISA is an enzyme-linked immunoassay designed for the in vitro measurement of S1P levels in human or animal biological fluids (blood, serum, synovial fluid, cell lysate, and tissue lysate).

Storage

Upon receipt, Part 1 of the S1P-ELISA kit must be stored at -20°C and Part 2 (TMB Substrate) must be stored at 4°C. Under proper storage conditions, the kit components are stable for at least 6 months from date of receipt. Opened and reconstituted solutions are less stable. All components and solutions should be protected from excessive light and heat.

General Description

Sphingosine 1-Phosphate (S1P) is a crucial bioactive lipid mediator and key component of the sphingolipid signaling cascade. S1P, produced by the enzymes, Sphingosine Kinase 1 and 2 (SphK1, SphK2), initiates a proliferative1, pro-angiogenic2, and anti-apoptotic3 sequence of events that contributes to the progression of cancer, diabetes, and osteoporosis. SphK1 has been shown to be up-regulated in a variety of cancers and recent research suggests that S1P itself, is a potent tumorigenic growth factor that may be a novel biomarker for early stage cancer detection4,5. S1P levels are tightly regulated by enzymes S1P Lyase (SPL), involved in its degradation, and two S1P-specific phosphatases and three lipid phosphatases that are involved in its synthesis. Additionally, S1P levels and its actions are controlled through a family of cell surface G protein receptors (S1PR1-5). These receptors have been implicated in a variety of developmental and disease related processes; such as immune6 and vascular regulation7. S1P is also known for its direct role as a second messenger during inflammation7 and the SPhK/S1P/S1P-receptor signaling family has been implicated in a variety of pathophysiological conditions and diseases such as atherosclerosis, cancer, diabetes, multiple sclerosis, sepsis, and so forth. Interference of these routes has the potential for the treatment of cancer, chronic inflammatory disorders and autoimmune diseases.

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Documents

pdf COA

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pdf Datasheet

QA & Reviews

Customer Reviews

References

Sphingosine kinase 1 is required for myristate-induced TNF alpha expression in intestinal epithelial cells

PROSTAGLANDINS & OTHER LIPID MEDIATORS

Authors: Choi, Songhwa; Snider, Justin M.; Cariello, Chris P.; Lambert, Johana M.; Anderson, Andrea K.; Cowart, L. Ashley; Snider, Ashley J.

Abstract

Saturated fatty acids (SFA) have been known to trigger inflammatory signaling in metabolic tissues; however, the effects of specific SFAs in the intestinal epithelium have not been well studied. Several previous studies have implicated disruptions in sphingolipid metabolism by oversupply of SFAs in inflammatory process. Also, our previous studies have implicated sphingosine kinase 1 (SK1) and its product sphingosine-1-phosphate (S1P) as having key roles in the regulation of inflammatory processes in the intestinal epithelium. Therefore, to define the role for specific SFAs in inflammatory responses in intestinal epithelial cells, we examined myristate (C14:0) and palmitate (C16:0). Myristate, but not palmitate, significantly induced the pro-inflammatory cytokine tumor necrosis factor alpha (TNF alpha), and it was SK1-dependent. Interestingly, myristate-induced TNF alpha expression was not suppressed by inhibition of S1P receptors (S1PRs), hinting at a potential novel intracellular target of S1P. Additionally, myristate regulated the expression of TNF alpha via JNK activation in an SK1-dependent manner, suggesting a novel S1PR-independent target as a mediator between SK1 and JNK in response to myristate. Lastly, a myristate-enriched milk fat-based diet (MFBD) increased expression of TNF alpha in colon tissues and elevated the S1P to sphingosine ratio, demonstrating the potential of myristate-involved pathobiologies in intestinal tissues. Taken together our studies suggest that myristate regulates the expression of TNF alpha in the intestinal epithelium via regulation of SK1 and JNK.

Workshop Report FDA Workshop on Improving Cardiotoxicity Assessment With Human-Relevant Platforms

CIRCULATION RESEARCH

Authors: Pang, Li; Sager, Philip; Yang, Xi; Shi, Hong; Sannajust, Frederick; Brock, Mathew; Wu, Joseph C.; Abi-Gerges, Najah; Lyn-Cook, Beverly; Berridge, Brian R.; Stockbridge, Norman

Abstract

Given that cardiovascular safety concerns remain the leading cause of drug attrition at the preclinical drug development stage, the National Center for Toxicological Research of the US Food and Drug Administration hosted a workshop to discuss current gaps and challenges in translating preclinical cardiovascular safety data to humans. This white paper summarizes the topics presented by speakers from academia, industry, and government intended to address the theme of improving cardiotoxicity assessment in drug development. The main conclusion is that to reduce cardiovascular safety liabilities of new therapeutic agents, there is an urgent need to integrate human-relevant platforms/approaches into drug development. Potential regulatory applications of human-derived cardiomyocytes and future directions in employing human-relevant platforms to fill the gaps and overcome barriers and challenges in preclinical cardiovascular safety assessment were discussed. This paper is intended to serve as an initial step in a public-private collaborative development program for human-relevant cardiotoxicity tools, particularly for cardiotoxicities characterized by contractile dysfunction or structural injury.