N-木香油基-D-赤型-鞘糖基磷酸胆碱 | 60037-60-7

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 鞘脂
• 中文名称: N-木香油基-D-赤型-鞘糖基磷酸胆碱
• 英文名称: SM (d18:1/24:0)
• 英文别名: C24 Sphingomyelin；[(E,2S,3R)-3-hydroxy-2-(tetracosanoylamino)octadec-4-enyl] 2-(trimethylazaniumyl)ethyl phosphate
• CAS: 60037-60-7
• 化学式: C₄₇H₉₅N₂O₆P
• 分子量: 815.255
• InChiKey: QEDPUVGSSDPBMD-XTAIVQBESA-N

计算性质

• 辛醇/水分配系数(LogP)：
  16.6
• 重原子数：
  56
• 可旋转键数：
  44
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.94
• 拓扑面积：
  108
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  N-木香油基-D-赤型-鞘糖基磷酸胆碱 在 palladium 10% on activated carbon 、 氢气 作用下， 以 甲醇 为溶剂， 生成 SM (d18:0/24:0)
  参考文献：
  名称：

  METHOD OF ISOLATING SPHINGOLIPIDS FROM CORDYCEPS AND THEIR USE

  摘要：

  一种从冬虫夏草中分离至少一种鞘脂成分的方法，所选的鞘脂成分包括鞘氨醇基部分、鞘烷酸酰胺部分、糖鞘脂部分或磷鞘脂部分，特别是从野生型冬虫夏草中分离，可获得含有鞘氨醇基、鞘烷酸酰胺、糖鞘脂或磷鞘脂中一种成分增加的鞘脂成分。分离的鞘脂成分中含有迄今未报告过的显着鞘脂成分，并具有特殊的免疫抑制活性。一种治疗患有自身免疫疾病或过敏疾病等炎症性疾病的受试者的方法，包括给受试者投与从冬虫夏草中分离的鞘脂。一种治疗患有炎症性疾病的受试者的方法，包括给受试者投与某些鞘脂。此外，根据本发明，还提供了一种组合物，特别是一种包含至少一种鞘脂成分的药物组合物。

  公开号：

  US20170128507A1
• 作为产物：
  描述：

  、 三甲胺 生成 N-木香油基-D-赤型-鞘糖基磷酸胆碱
  参考文献：
  名称：

  Studies on Sphingolipids. VII. Synthesis and Configuration of Natural Sphingomyelins

  摘要：

  DOI：

  10.1021/ja00865a036

文献信息

• Role for Mammalian Neutral Sphingomyelinase 2 in Confluence-induced Growth Arrest of MCF7 Cells
  作者：Norma Marchesini、Walid Osta、Jacek Bielawski、Chiara Luberto、Lina M. Obeid、Yusuf A. Hannun

  DOI：10.1074/jbc.m313662200

  日期：2004.6

  Recently, we reported that neutral sphingomyelinase 2 (nSMase2) functions as a bona fide neutral sphingomyelinase and that overexpression of nSMase2 in MCF7 breast cancer cells caused a decrease in cell growth (Marchesini, N., Luberto, C., and Hannun, Y. A. (2003) J. Biol. Chem. 278, 13775-13783). In this study, the role of endogenous nSMase2 in regulating growth arrest was investigated. The results show that endogenous nSMase2 mRNA was up-regulated similar to5-fold when MCF7 cells became growth-arrested at confluence, and total neutral SMase activity was increased by 119 +/- 41% with respect to control. Cell cycle analysis showed that up-regulation of endogenous nSMase2 correlated with G(0)/G(1) cell cycle arrest and an increase in total ceramide levels (2.4-fold). Analysis of ceramide species showed that confluence caused selective increases in very long chain ceramide C-24:1 (370 +/- 54%) and C-24:0 (266 +/- 81%) during arrest. The role of endogenous nSMase2 in growth regulation and ceramide metabolism was investigated using short interfering RNA (siRNA)-mediated loss-of-function analysis. Down-regulation of nSMase2 with specific siRNA increased the cell population of cells in S phase of the cell cycle by 59 +/- 14% and selectively reverted the effects of growth arrest on the increase in levels of very long chain ceramides. Mechanistically, confluence arrest also induced hypophosphorylation of the retinoblastoma protein (6-fold) and induction of p21(WAF1) (3-fold). Downregulation of nSMase2 with siRNA largely prevented the dephosphorylation of the retinoblastoma protein and the induction of p21(WAF1), providing a link between the action of nSMase2 and key regulators of cell cycle progression. Moreover, studies on nSMase2 localization in MCF7 cells showed that nSMase2 distributed throughout the cells in subconfluent, proliferating cultures. In contrast, nSMase2 became nearly exclusively located at the plasma membrane in confluent, contact-inhibited cells. Hence, we demonstrate for the first time that nSMase2 functions as a growth suppressor in MCF7 cells, linking confluence to the G(0)/G(1) cell cycle check point.