Sphinganine (d18:0)
(Synonyms: D-赤式-C18-二氢-D-神经鞘氨醇) 目录号 : GC40794Sphingolipid pathway intermediate
Cas No.:764-22-7
Sample solution is provided at 25 µL, 10mM.
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- Purity: ≥95.00%
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Sphinganine (d18:0) is a precursor of ceramide and sphingosine as well as a substrate of sphingosine kinases, which generate sphinganine-1-phosphate. Sphinganine levels increase significantly in response to certain mycotoxins, including fumonisins,[1,2] as well as in some cancers.[3] Sphinganine can block protein kinase C activation in some cases but not others.[4,5] Sphinganine-1-phosphate can emulate sphingosine-1-phosphate in cell signaling or have opposite intracellular effects.[6,7,8]
References:
1. Pruett, S.T., Bushnev, A., Hagedorn, K., et al. Biodiversity of sphingoid bases ("sphingosines") and related amino alcohols. J. Lipid Res. 49(8), 1621-1639 (2008).
2. Shephard, G.S., van der Westhuizen, L., and Sewram, V. Biomarkers of exposure to fumonisin mycotoxins: A review. Food Addit. Contam. 24(10), 1196-1201 (2007).
3. Yin, J., Miyazaki, K., Shaner, R.L., et al. Altered sphingolipid metabolism induced by tumor hypoxia - new vistas in glycolipid tumor markers. FEBS Lett. 584(9), 1872-1878 (2010).
4. Merrill, A.H., Jr., Sereni, A.M., Stevens, V.L., et al. Inhibition of phorbol ester-dependent differentiation of human promyelocytic leukemic (HL-60) cells by sphinganine and other long-chain bases. J. Biol. Chem. 261(27), 12610-12615 (1986).
5. Merrill, A.H., Jr., Nimkar, S., Menaldino, D., et al. Structural requirements for long-chain (shingoid) base inhibition of protein kinase C in vitro and for the cellular effects of these compounds. Biochemistry 28(8), 3138-3145 (1989).
6. Coste, O., Brenneis, C., Linke, B., et al. Sphingosine 1-phosphate modulates spinal nociceptive processing. J. Biol. Chem. 283(47), 32442-32451 (2008).
7. Bu, S., Yamanaka, M., Pei, H., et al. Dihydrosphingosine 1-phosphate stimulates MMP1 gene expression via activation of ERK1/2-Ets1 pathway in human fibroblasts. FASEB J. 20(1), 184-186 (2006).
8. Bu, S., Kapanadze, B., Hsu, T., et al. Opposite effects of dihydrosphingosine 1-phosphate and sphingosine 1-phosphate on transforming growth factor-β/Smad signaling are mediated through the PTEN/PPM1A-dependent pathway. J. Biol. Chem. 283(28), 19593-19602 (2008).
Cas No. | 764-22-7 | SDF | |
别名 | D-赤式-C18-二氢-D-神经鞘氨醇 | ||
Canonical SMILES | OC[C@H](N)[C@H](O)CCCCCCCCCCCCCCC | ||
分子式 | C18H39NO2 | 分子量 | 301.5 |
溶解度 | DMF: 10 mg/ml,DMSO: 2 mg/ml,Ethanol: Miscible | 储存条件 | Store at -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
制备储备液 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 3.3167 mL | 16.5837 mL | 33.1675 mL |
5 mM | 0.6633 mL | 3.3167 mL | 6.6335 mL |
10 mM | 0.3317 mL | 1.6584 mL | 3.3167 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
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DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
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Palmitoyl-ceramide accumulation with necrotic cell death in A549 cells, followed by a steep increase in Sphinganine content
Biochim Open 2015 Jun 21;1:11-27.PMID:29632826DOI:10.1016/j.biopen.2015.06.001.
Ceramides (Cers) have recently been identified as key signaling molecules that mediate biological functions such as cell growth, differentiation, senescence, apoptosis, and autophagy. However, the functions of Cer accumulation in necrotic cell death remain unknown. The aim of this study was to clarify the relationship between Cer accumulation with inhibition of the conversion pathway of Cer and concomitant necrotic cell death. In order to minimize the effect of apoptosis against necrotic cell death, A549 cells having the inhibiting effect of caspase 9 by survivin were used in this study. Consequently, Cer accumulation in A549 cells would likely be associated with a pathway other than the mitochondrial caspase-dependent pathway of apoptosis. Here, we showed that the dual addition of a glucosyl-Cer synthase inhibitor and a ceramidase inhibitor to A549 cell culture induced palmitoyl-Cer accumulation with Cer synthase 5 expression and necrotic cell death with lysosomal rupture together with leakage of cathepsin B/alkalization after 2-3 h, although it is unknown in this study whether the necrotic cell death was caused by the lysosomal rupture. This Cer accumulation was followed by a steep increase in Sphinganine base levels via the activation of serine palmitoyltransferase activity brought about by the increase in palmitoyl-coenzyme A concentration as a substrate after 5-6 h. The increase in palmitoyl-coenzyme A concentration was achieved by activation of the fatty acid synthetic pathway from acetyl coenzyme A.