血小板-活化因子C18 | 79549-26-1

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 甘油磷脂
• 中文名称: 血小板-活化因子C18
• 中文别名: 血小板-活化因子C18
• 英文名称: 1-Octadecanoyl-2-acetyl-sn-glycero-3-phosphocholine
• 英文别名: [(2R)-2-acetyloxy-3-octadecanoyloxypropyl] 2-(trimethylazaniumyl)ethyl phosphate
• CAS: 79549-26-1
• 化学式: C28H56NO8P
• 分子量: 565.7
• InChiKey: ILLILTKBYHPOIA-HHHXNRCGSA-N

物化性质

• 溶解度：
  在氯仿中的溶解度为10 mg/mL

计算性质

• 辛醇/水分配系数(LogP)：
  7.2
• 重原子数：
  38
• 可旋转键数：
  28
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.93
• 拓扑面积：
  111
• 氢给体数：
  0
• 氢受体数：
  8

反应信息

• 作为反应物：
  描述：

  血小板-活化因子C18 、 水 生成 硬脂酰溶血卵磷脂 、 乙酸盐 、 氢(+1)阳离子
  参考文献：
  名称：

  Metabolomics annotates ABHD3 as a physiologic regulator of medium-chain phospholipids

  摘要：

  一种非靶向代谢组学方法发现，C14磷脂酰胆碱（PC）是脂肪酶ABHD3的特异性细胞中链底物，还发现了C5âC8短链PC，包括氧化的促动脉粥样硬化和促凋亡PC磷脂。 包括人类在内的所有生物体都拥有大量未定性的酶。在这里，我们描述了一种通过非靶向代谢组学发现酶底物的通用细胞筛选方法，以及该方法在鉴定含δ/δ²-水解酶结构域的蛋白δ/δ²-水解酶结构域3（ABHD3）的应用，该蛋白δ/δ²-水解酶结构域3（ABHD3）是一种选择性裂解中链和氧化截短磷脂的脂肪酶。ABHD3â/â小鼠的肉豆蔻酰（C14）-磷脂含量升高，其中包括生物活性脂质C14-赖磷脂酰胆碱，这证实了我们底物分配的生理相关性。

  DOI：

  10.1038/nchembio.659
• 作为产物：
  描述：

  硬脂酰溶血卵磷脂 、 (2R)-N-[3-(2-acetylsulfanylethylimino)-3-oxidopropyl]-4-[[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-4-hydroxy-3-phosphonatooxyoxolan-2-yl]methoxy-hydroxyphosphoryl]oxy-hydroxyphosphoryl]oxy-2-hydroxy-3,3-dimethylbutanimidate 生成 血小板-活化因子C18 、 coenzyme A
  参考文献：
  名称：

  A Single Enzyme Catalyzes Both Platelet-activating Factor Production and Membrane Biogenesis of Inflammatory Cells

  摘要：

  Platelet-activating factor (PAF) is a potent proinflammatory lipid mediator eliciting a variety of cellular functions. Lipid mediators, including PAF are produced from membrane phospholipids by enzymatic cascades. Although a G protein-coupled PAF receptor and degradation enzymes have been cloned and characterized, the PAF biosynthetic enzyme, aceyl-CoAdyso-PAF acetyltransferase, has not been identified. Here, we cloned lyso-PAF acetyltransferase, which is critical in stimulus-dependent formation of PAF. The enzyme is a 60-kDa microsomal protein with three putative membrane-spanning domains. The enzyme was induced by bacterial endotoxin (lipopolysaccharide), which was suppressed by dexamethasone treatment. Surprisingly, the enzyme catalyzed not only biosynthesis of PAF from lyso-PAF but also incorporation of arachidonoyl-CoA to produce PAF precursor membrane glycerophospholipids (lysophosphatidylcholine acyltransferase activity). Under resting conditions, the enzyme prefers arachidonoyl-CoA and contributes to membrane biogenesis. Upon acute inflammatory stimulation with lipopolysaccharide, the activated enzyme utilizes acetyl-CoA more efficiently and produces PAF. Thus, our findings provide a novel concept that a single enzyme catalyzes membrane biogenesis of inflammatory cells while producing prophlogistic mediator in response to external stimuli.

  DOI：

  10.1074/jbc.m609641200