18:0溶血剂PE | 69747-55-3

• 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: 18:0溶血剂PE
• 中文别名: 1-硬脂酰基-2-羟基-sn-甘油-3-磷酸乙醇胺；1-十六烷酰基-sn-甘油-3-磷酸乙醇胺;PE（18：0/0：0）;11070
• 英文名称: LysoPE (18:0/0:0)
• 英文别名: 18:0 LPE；1-Stearoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine；2-azaniumylethyl [(2R)-2-hydroxy-3-octadecanoyloxypropyl] phosphate
• CAS: 69747-55-3
• 化学式: C₂₃H₄₈NO₇P
• 分子量: 481.61
• InChiKey: BBYWOYAFBUOUFP-JOCHJYFZSA-N

物化性质

• 沸点：
  597.3±60.0 °C(Predicted)
• 密度：
  1.075±0.06 g/cm3(Predicted)
• 溶解度：
  氯仿：可溶； DMF：可溶；二甲基亚砜：可溶
• 物理描述：
  Solid

计算性质

• 辛醇/水分配系数(LogP)：
  3.4
• 重原子数：
  32
• 可旋转键数：
  25
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.96
• 拓扑面积：
  128
• 氢给体数：
  3
• 氢受体数：
  8

制备方法与用途

生物活性

18:0 LYSO-PE 是一种可以诱导 [Ca²⁺]i 增加的化合物。

体外研究

在 SK-OV3 细胞和 PC-12 细胞中，18:0 LYSO-PE 能够引起 [Ca²⁺]i 的增加；但在 MDA-MB-231 细胞中则未观察到此现象。

反应信息

• 作为反应物：
  描述：

  18:0溶血剂PE 在 4-二甲氨基吡啶 、 sodium carbonate 、 溶剂黄146 、 三乙胺 、 N,N'-二环己基碳二亚胺 作用下， 以 四氢呋喃 、 水 为溶剂， 反应 24.0h， 生成
  参考文献：
  名称：

  Yoneda, Kenji; Sasakura, Keiji; Tahara, Shoichi, Angewandte Chemie, 1992, vol. 104, # 10, p. 1386 - 1387

  摘要：

  DOI：
• 作为产物：
  描述：

  (S)-1-硬脂酰-2-O-苄基-锡-甘油 在 palladium dihydroxide oxonium 、 氢气 、 三氯氧磷 作用下， 生成 18:0溶血剂PE
  参考文献：
  名称：

  Yoneda, Kenji; Sasakura, Keiji; Tahara, Shoichi, Angewandte Chemie, 1992, vol. 104, # 10, p. 1386 - 1387

  摘要：

  DOI：

文献信息

• Discovery of a lysophospholipid acyltransferase family essential for membrane asymmetry and diversity
  作者：Daisuke Hishikawa、Hideo Shindou、Saori Kobayashi、Hiroki Nakanishi、Ryo Taguchi、Takao Shimizu

  DOI：10.1073/pnas.0712245105

  日期：2008.2.26

  All organisms consist of cells that are enclosed by a cell membrane containing bipolar lipids and proteins. Glycerophospholipids are important not only as structural and functional components of cellular membrane but also as precursors of various lipid mediators. Polyunsaturated fatty acids comprising arachidonic acid or eicosapentaenoic acid are located at sn -2 position, but not at sn -1 position of glycerophospholipids in an asymmetrical manner. In addition to the asymmetry, the membrane diversity is important for membrane fluidity and curvature. To explain the asymmetrical distribution of fatty acids, the rapid turnover of sn -2 position was proposed in 1958 by Lands [Lands WE (1958) Metabolism of glycerolipides: A comparison of lecithin and triglyceride synthesis. J Biol Chem 231:883–888]. However, the molecular mechanisms and biological significance of the asymmetry remained unknown. Here, we describe a putative enzyme superfamily consisting mainly of three gene families, which catalyzes the transfer of acyl-CoAs to lysophospholipids to produce different classes of phospholipids. Among them, we characterized three important enzymes with different substrate specificities and tissue distributions; one, termed lysophosphatidylcholine acyltransferase-3 (a mammalian homologue of Drosophila nessy critical for embryogenesis), prefers arachidonoyl-CoA, and the other two enzymes incorporate oleoyl-CoAs to lysophosphatidylethanolamine and lysophosphatidylserine. Thus, we propose that the membrane diversity is produced by the concerted and overlapped reactions with multiple enzymes that recognize both the polar head group of glycerophospholipids and various acyl-CoAs. Our findings constitute a critical milestone for our understanding about how membrane diversity and asymmetry are established and their biological significance.

  所有生物体都由细胞组成，这些细胞被包含双极脂质和蛋白质的细胞膜所包围。甘油磷脂不仅作为细胞膜的结构和功能组成部分，还是各种脂质介质的前体。由花生四烯酸或二十碳五烯酸组成的多不饱和脂肪酸位于甘油磷脂的不对称的sn-2位置，而不是sn-1位置。除了不对称性外，膜的多样性对于膜的流动性和曲率也很重要。为了解释脂肪酸的不对称分布，1958年Lands提出了sn-2位置的快速周转。然而，不对称性的分子机制和生物学意义仍然未知。在这里，我们描述了一个潜在的酶超家族，主要由三个基因家族组成，它们催化酰基辅酶A转移至溶血磷脂，以产生不同类别的磷脂。其中，我们表征了三种具有不同底物特异性和组织分布的重要酶；一种被称为溶血磷脂酰转移酶-3（果蝇nessy的哺乳动物同源物，对胚胎发育至关重要），更喜欢花生四烯酰辅酶A，而另外两种酶则将油酰辅酶A并入到溶血磷脂酰乙醇胺和溶血磷脂酰丝氨酸中。因此，我们提出，膜的多样性是由多个酶的协同和重叠反应产生的，这些酶识别甘油磷脂的极性头基和各种酰基辅酶A。我们的发现对于我们理解膜的多样性和不对称性的建立及其生物学意义构成了一个关键的里程碑。
• Roles of C-Terminal Processing, and Involvement in Transacylation Reaction of Human Group IVC Phospholipase A2 (cPLA2γ)
  作者：Atsushi Yamashita、Ryo Kamata、Norikazu Kawagishi、Hiroki Nakanishi、Hiroshi Suzuki、Takayuki Sugiura、Keizo Waku

  DOI：10.1093/jb/mvi067

  日期：2005.5.1

  The phospholipase A2s (PLA2s) are a diverse group of enzymes that hydrolyze the sn-2 fatty acid from phospholipids and play a role in a wide range of physiological functions. A 61-kDa calcium-independent PLA2, termed cPLA2γ, was identified as an ortholog of cPLA2α with approximately 30% overall sequence identity. cPLA2γ contains a potential prenylation motif at its C terminus, and is known to have PLA2 and lysophospholipase activities, but its physiological roles have not been clarified. In the present study, we expressed various forms of recombinant cPLA2γ, including non-prenylated and non-cleaved forms, in order to investigate the effects of C-terminal processing. We examined the expression of the wild type and non-prenylated (SCLA) forms of cPLA2γ, and found that the SCLA form was expressed normally and retained almost full activity. Expression of the prenylated and non-cleaved form of cPLA2γ using yeast mutants lacking prenyl protein proteases AFC1 (a-factor–converting enzyme) and RCE1 (Ras-converting enzyme) revealed decreased expression in the mutant strain compared to that in the wild type yeast, suggesting that complete C-terminal processing is important for the functional expression of cPLA2γ. In addition, cPLA2γ was found to have coenzyme A (CoA)–independent transacylation and lysophospholipid (LPL) dismutase (LPLase/transacylase) activities, suggesting that it may be involved in fatty acid remodeling of phospholipids and the clearance of toxic lysophospholipids in cells.

  磷脂酶 A2（PLA2）是一类多种多样的酶，能水解磷脂中的 sn-2 脂肪酸，在多种生理功能中发挥作用。cPLA2γ 在其 C 端含有一个潜在的前酰化基团，已知具有 PLA2 和溶血磷脂酶活性，但其生理作用尚未明确。在本研究中，我们表达了各种形式的重组 cPLA2γ，包括非前酰化和非裂解形式，以研究 C 端加工的影响。我们检测了野生型和非肾上腺素化（SCLA）型 cPLA2γ 的表达，发现 SCLA 型表达正常，几乎保持了全部活性。利用缺乏前炔蛋白蛋白酶 AFC1（a-因子转换酶）和 RCE1（Ras 转换酶）的酵母突变体表达前炔化和非裂解形式的 cPLA2γ，发现与野生型酵母相比，突变株的表达量减少，这表明完整的 C 端处理对 cPLA2γ 的功能表达很重要。此外，还发现 cPLA2γ 具有独立于辅酶 A（CoA）的反酰化和溶血磷脂（LPL）歧化酶（LPLase/transacylase）活性，这表明它可能参与了磷脂的脂肪酸重塑和细胞中有毒溶血磷脂的清除。
• Gas-filled stabilized particles and methods of use
  申请人：Children's Medical Center Corporation

  公开号：US10577554B2

  公开（公告）日：2020-03-03

  Provided herein are various gas-filled particles having a stabilized membrane that encapsulates the gas. Pharmaceutical compositions, methods of use and treatment, and methods of preparation are also described.

  本文提供了各种充满气体的颗粒，这些颗粒具有封装气体的稳定膜。此外，还介绍了药物组合物、使用和处理方法以及制备方法。
• Subcellular localization and lysophospholipase/transacylation activities of human group IVC phospholipase A2 (cPLA2γ)
  作者：Atsushi Yamashita、Ken Tanaka、Ryo Kamata、Tsukasa Kumazawa、Naotaka Suzuki、Hiroki Koga、Keizo Waku、Takayuki Sugiura

  DOI：10.1016/j.bbalip.2009.05.008

  日期：2009.10

  cPLA2 gamma was identified as an ortholog of cPLA2 alpha, which is a key enzyme in eicosanoid production. cPLA2 gamma was reported to be located in endoplasmic reticulum (ER) and mitochondria and to have lysophospholipase activity beside phospholipase A2 (PLA2) activity. However, subcellular localization, mechanism of membrane binding, regulation and physiological function have not been fully established. In the present study, we examined the subcellular localization and enzymatic properties of cPLA2 gamma with C-terminal FLAG-tag. We found that cPLA2 gamma was located not only in ER but also mitochondria even in the absence of the prenylation. Purified recombinant cPLA2 gamma catalyzed an acyltransferase reaction from one molecule of lysophosphatidylcholine (LPC) to another, forming phosphatidylcholine (PC). LPC or lysophosphatidylethanolamine acted as acyl donor and acceptor, but lysophosphatidylserine, lysophosphatidylinositol and lysophosphatidic acid (LPA) did not. PC and phosphatidylethanolamine (PE) also acted as weak acyl donors. Reaction conditions changed the balance of lysophospholipase and transacylation activities, with addition of LPA/PA, pH>8, and elevated temperature markedly increasing transacylation activity; this suggests that lysophospholipase/transacylation activities of cPLA2 gamma may be regulated by various factors. As lysophospholipids are known to accumulate in ischemia heart and to induce arryhthmia, the cPLA2 gamma that is abundant in heart may have a protective role through clearance of lysophospholipids by its transacylation activity. (C) 2009 Elsevier B.V. All rights reserved.
• Group VIA Phospholipase A2 Mitigates Palmitate-induced β-Cell Mitochondrial Injury and Apoptosis
  作者：Haowei Song、Mary Wohltmann、Min Tan、Jack H. Ladenson、John Turk

  DOI：10.1074/jbc.m114.561910

  日期：2014.5

  Background: Lipid-induced -cell loss contributes to type 2 diabetes mellitus (T2DM). Results: Palmitate-induced -cell lipid oxidation, mitochondrial dysfunction, and apoptosis correlate inversely with expression of iPLA(2), which associates with mitochondria, generates monolysocardiolipin, and lowers oxidized phospholipid content. Conclusion: iPLA(2) mitigates palmitate-induced -cell mitochondrial injury and apoptosis and may facilitate repair of oxidized lipids. Significance: Understanding lipid-induced -cell loss could lead to T2DM therapies.Palmitate (C16:0) induces apoptosis of insulin-secreting -cells by processes that involve generation of reactive oxygen species, and chronically elevated blood long chain free fatty acid levels are thought to contribute to -cell lipotoxicity and the development of diabetes mellitus. Group VIA phospholipase A(2) (iPLA(2)) affects -cell sensitivity to apoptosis, and here we examined iPLA(2) effects on events that occur in -cells incubated with C16:0. Such events in INS-1 insulinoma cells were found to include activation of caspase-3, expression of stress response genes (C/EBP homologous protein and activating transcription factor 4), accumulation of ceramide, loss of mitochondrial membrane potential, and apoptosis. All of these responses were blunted in INS-1 cells that overexpress iPLA(2), which has been proposed to facilitate repair of oxidized mitochondrial phospholipids, e.g. cardiolipin (CL), by excising oxidized polyunsaturated fatty acid residues, e.g. linoleate (C18:2), to yield lysophospholipids, e.g. monolysocardiolipin (MLCL), that can be reacylated to regenerate the native phospholipid structures. Here the MLCL content of mouse pancreatic islets was found to rise with increasing iPLA(2) expression, and recombinant iPLA(2) hydrolyzed CL to MLCL and released oxygenated C18:2 residues from oxidized CL in preference to native C18:2. C16:0 induced accumulation of oxidized CL species and of the oxidized phospholipid (C18:0/hydroxyeicosatetraenoic acid)-glycerophosphoethanolamine, and these effects were blunted in INS-1 cells that overexpress iPLA(2), consistent with iPLA(2)-mediated removal of oxidized phospholipids. C16:0 also induced iPLA(2) association with INS-1 cell mitochondria, consistent with a role in mitochondrial repair. These findings indicate that iPLA(2) confers significant protection of -cells against C16:0-induced injury.