(2E)-decenoyl-coenzyme A | 10018-95-8

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: (2E)-decenoyl-coenzyme A
• 英文别名: 2-trans-decenoyl-CoA；trans-2-decenoyl CoA；trans-2-decenoyl-CoA；(2E)-2-decenoyl-CoA；trans-Dec-2-enoyl-CoA；S-[2-[3-[[(2R)-4-[[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-4-hydroxy-3-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl]oxy-hydroxyphosphoryl]oxy-2-hydroxy-3,3-dimethylbutanoyl]amino]propanoylamino]ethyl] (E)-dec-2-enethioate
• CAS: 10018-95-8
• 化学式: C₃₁H₅₂N₇O₁₇P₃S
• 分子量: 919.778
• InChiKey: MGNBGCRQQFMNBM-YJHHLLFWSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -1.7
• 重原子数：
  59
• 可旋转键数：
  27
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.68
• 拓扑面积：
  389
• 氢给体数：
  9
• 氢受体数：
  22

反应信息

• 作为产物：
  描述：

  trans-3-decenoylcoenzyme A 在 Drosophila melanogaster multifunctional enzyme type 2 、 wild type full length variant of human Δ³,Δ²-enoyl-coenzyme A isomerase type 2 、 β-烟酰胺腺嘌呤二核苷酸 作用下， 以 aq. buffer 为溶剂， 生成 (2E)-decenoyl-coenzyme A
  参考文献：
  名称：

  人Δ3，Δ2-烯酰基-CoA异构酶，类型2：结构酶学研究其ACBP域和helix-10的催化作用

  摘要：

  三聚体的人的催化结构域Δ 3，Δ 2烯酰基-CoA异构酶2型（HsECI2）具有典型的巴豆酶折叠。在该折叠的活性部位，两个主链NH基团形成一个氧阴离子孔，用于结合3E-或3Z-烯酰基-CoA底物分子的硫酯氧。谷氨酸催化对于在底物C2和C4原子之间进行质子转移以形成2E-烯酰基-CoA产物至关重要，该产物是β-氧化途径的关键中间体。活动站点被C端螺旋10覆盖。在HsECI2中，异构酶结构域在其N末端被一个酰基辅酶A结合蛋白（ACBP）域扩展。HsECI2的小角X射线散射分析表明，ACBP结构域突出于中央异构酶三聚体。异构酶结构域三聚体的X射线晶体学确定了活性位点的几何形状。一条隧道，由loop-2形成并从催化位点扩展到本体溶剂，表明脂肪酰基链的可能结合方式。量热数据显示，单独表达的ACBP和异构酶结构域与脂肪酰基CoA分子紧密结合。截短的异构酶变体（无ACBP域）具有明显的烯酰辅酶A异构酶活

  DOI：

  10.1111/febs.13179

文献信息

• Multiplexing of Combinatorial Chemistry in Antimycin Biosynthesis: Expansion of Molecular Diversity and Utility
  作者：Yan Yan、Jing Chen、Lihan Zhang、Qingfei Zheng、Ying Han、Hua Zhang、Daozhong Zhang、Takayoshi Awakawa、Ikuro Abe、Wen Liu

  DOI：10.1002/anie.201305569

  日期：2013.11.18

  Diversity‐oriented biosynthesis of a library of antimycin‐like compounds (380 altogether) was accomplished by using multiplex combinatorial biosynthesis. The core strategy depends on the use of combinatorial chemistry at different biosynthetic stages. This approach is applicable for the diversification of polyketides, nonribosomal peptides, and the hybrids that share a similar biosynthetic logic.

  通过使用多重组合生物合成，完成了抗霉素样化合物库（共380个）的面向多样性的生物合成。核心策略取决于在不同生物合成阶段使用组合化学。该方法适用于聚酮化合物，非核糖体肽以及具有相似生物合成逻辑的杂种的多样化。
• Inactivation of Thiolase by 2-Alkynoyl-CoA via Its Intrinsic Isomerase Activity
  作者：Long Wu、Jia Zeng、Guisheng Deng、Fei Guo、Nan Li、Xiaojun Liu、Xiusheng Chu、Ding Li

  DOI：10.1021/ol0712677

  日期：2007.9.1

  Selective inactivation of cytosolic thiolase by 2-alkynoyi-CoA via its intrinsic isomerase activity was studied, which provides an example for rationally developing mechanism-based inhibitors based on a side activity of the enzyme, and may become a supplemental method for better treatment of cardiovascular disease and cancer.
• Identification of Compounds with Potential Antibacterial Activity against <i>Mycobacterium</i> through Structure-Based Drug Screening
  作者：Tomohiro Kinjo、Yuji Koseki、Maiko Kobayashi、Atsumi Yamada、Koji Morita、Kento Yamaguchi、Ryoya Tsurusawa、Gulcin Gulten、Hideyuki Komatsu、Hiroshi Sakamoto、James C. Sacchettini、Mitsuru Kitamura、Shunsuke Aoki

  DOI：10.1021/ci300571n

  日期：2013.5.24

  To identify novel antibiotics against Mycobacterium tuberculosis, we performed a hierarchical structure-based drug screening (SBDS) targeting the enoyl-acyl carrier protein reductase (InhA) with a compound library of 154,118 chemicals. We then evaluated whether the candidate hit compounds exhibited inhibitory effects on the growth of two model mycobacterial strains: Mycobacterium smegmatis and Mycobacterium vanbaalenii. Two compounds (KE3 and KE4) showed potent inhibitory effects against both model mycobacterial strains. In addition, we rescreened KE4 analogs, which were identified from a compound library of 461,383 chemicals through fingerprint analysis and genetic algorithm-based docking simulations. All of the KE4 analogs (KES1 - KES5) exhibited inhibitory effects on the growth of M. smegmatis and/or M. vanbaalenii. Based on the predicted binding modes, we probed the structure-activity relationships of KE4 and its analogs and found a correlative relationship between the IC50 values and the interaction residues/LogP values. The most potent inhibitor, compound KES4, strongly and stably inhibited the long-term growth of the model bacteria and showed higher inhibitory effects (IC50 = 4.8 mu M) than isoniazid (IC50 = 5.4 mu M), which is a first-line drug for tuberculosis therapy. Moreover, compound KES4 did not exhibit any toxic effects that impede cell growth in several mammalian cell lines and enterobacteria. The structural and experimental information of these novel chemical compounds will likely be useful for the development of new anti-TB drugs. Furthermore, the methodology that was used for the identification of the effective chemical compound is also likely to be effective in the SBDS of other candidate medicinal drugs.
• Metabolomics-Based Identification of Disease-Causing Agents
  申请人：Skolnick Jeffrey

  公开号：US20110246081A1

  公开（公告）日：2011-10-06

  A method, computer-readable medium, and system for identifying one or more metabolites associated with a disease, comprising: comparing gene expression data from diseased cells to gene expression data from control cells in order to deduce genes that are differentially-regulated in the diseased cells relative to the control cells; based on enzyme function and pathway data for all human metabolites that utilize the genes that are differentially-regulated in the disease cells, identifying one or more metabolites whose intracellular levels are higher or lower in diseased cells than in control cells, and thereby associating the one or more metabolites with the disease.
• [EN] METABOLOMICS-BASED IDENTIFICATION OF DISEASE-CAUSING AGENTS<br/>[FR] IDENTIFICATION D'AGENTS PROVOQUANT UNE MALADIE BASÉE SUR LA MÉTABOLOMIQUE
  申请人：GEORGIA TECH RES INST

  公开号：WO2009052186A1

  公开（公告）日：2009-04-23

  A method, computer-readable medium, and system for identifying one or more metabolites associated with a disease, comprising: comparing gene expression data from diseased cells to gene expression data from control cells in order to deduce genes that are differentially-regulated in the diseased cells relative to the control cells; based on enzyme function and pathway data for all human metabolites that utilize the genes that are differentially-regulated in the disease cells, identifying one or more metabolites whose intracellular levels are higher or lower in diseased cells than in control cells, and thereby associating the one or more metabolites with the disease.