| 包装 | 价格(元) |
| 10mM (in 1mL EtOH) | 电议 |
| 10mg | 电议 |
Preparation Method | The protein-kinase assay was carried out in a total volume of 50μL containing 5μL of sphingosine (D-erythro-sphingosine) suspension (or ethanol solution), 5μL of other effectors, 20μL Mg2+/ATP solution (100mM Tris/HCl, pH 7.4, 25mM MgCl2, 62.5μM ATP and 62.5μCi/mL [32P]ATP) and 20μL of diluted cytosol (8-12μg of protein per sample). |
Reaction Conditions | 0-100μM D-erythro-sphingosine |
Applications | When D-erythro-sphingosine was added to cytosolic extracts of Jurkat T cells, it caused a concentration-dependent phosphorylation of a p32 protein, suggesting that a p32-sphingosine-activated protein kinase was being activated. D-erythro-Sphingosine caused an approx.4-fold increase in p32 phosphorylation, with maximal effects observed at a concentration of 10μM of sphingosine. The EC50for D-erythro-sphingosine was 8μM. |
Cell lines | HEK293 cells |
Preparation Method | D-erythro-Sphingosine were diluted from 20mM stock solutions in ethanol. |
Reaction Conditions | 20μM D-erythro-Sphingosine |
Applications | Extracellular application of D-erythro-Sphingosine induced an increase in [Ca2+]i in TRPM3-transfected HEK293 cells within 20 to 30s after start of application. In fura-2 quench experiments using 200μM Mn2+, the spontaneous activity of TRPM3-transfected HEK293 cells was enhanced after application of D-erythro-Sphingosine. The concentration of D-erythro-Sphingosine for half-maximal activation of TRPM3 was 12μM obtained from increases in [Ca2+]i. Application of D-erythro-Sphingosine as well as application of hypotonic extracellular solution each produced increases in [Ca2+]i with comparable amplitudes in individual cells. |
| 产品描述 | D-erythro-sphingosine (Erythrosphingosine) is a very potent activator of p32-kinase with an EC50value of 8μM[1]. D-erythro-Sphingosine is also a PP2A agonist[2]. D-erythro-sphingosine has been shown to inhibit protein kinase C[3]. D-erythro-sphingosine activated TRPM3 variant containing 1325 aa, independently of PKC inhibition, formation of S1P, or intracellular Ca2+store depletion[4]. D-erythro-sphingosine lowered the levels of HMG-CoA reductase activity in CHO-K1 cells[5]. D-erythro-sphingosine significantly inhibited mastoparan-, but not Na3VO4-, stimulated arachidonic acid release in PC12 cells. Production of prostaglandin F2αwas suppressed by D-erythro-sphingosine (10 μM) in PC12 cells. D-erythro-sphingosine, directly inhibited cytosolic phospholipase A2αactivity[6]. A p32-sphingosine-activated protein kinase responded to low concentrations of D-erythro-sphingosine with an initial activation observed at 2.5μM and a peak activity at 10-20μM. This kinase showed a modest specificity for D-erythro-sphingosine over other sphingosine stereoisomers, and a preference for sphingosines over dihydro-sphingosines[1] D-erythro-sphingosine was identified as one of the most influential factors in ASB-induced nephrotoxicity[7] References: |
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