Myristic Acid Alkyne
(Synonyms: 13-十四炔酸,13-alkyne Myristic Acid) 目录号 : GC44258
Myristic acid containing an ω-terminal alkyne
Cas No.:82909-47-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Myristic acid is a 14-carbon saturated (14:0) fatty acid. In vivo, it is commonly added covalently to the N-terminus of proteins in a co-translational process termed N-myristoylation. [1] The sirtuin SIRT6 removes this acyl group from myristoylated TNF-α, enhancing secretion.[2] Myristic acid alkyne is a form of this myristic acid with an ω-terminal alkyne. Such terminal alkyne groups can be used in linking reactions, known as click chemistry, characterized by high dependability and specificity of azide-alkyne bioconjugation reactions. [3][4]Click chemistry has only recently been applied to the study of lipids.[2][5]
Reference:
[1]. Farazi, T.A., Waksman, G., and Gordon, J.I. The biology and enzymology of protein N-myristoylation. The Journal of Biological Chemisty 276(43), 39501-39504 (2001).
[2]. Jiang, H., Khan, S., Wang, Y., et al. SIRT6 regulates TNF-α secretion through hydrolysis of long-chain fatty acyl lysine. Nature 496, 110-113 (2013).
[3]. Kolb, H.C., and Sharpless, K.B. The growing impact of click chemistry on drug discovery. Drug Discov. Today 8(24), 1128-1137 (2003).
[4]. Lutz, J.F., and Zarafshani, Z. Efficient construction of therapeutics, bioconjugates, biomaterials and bioactive surfaces using azide-alkyne "click" chemistry. Adv. Drug Deliv. Rev. 60(9), 958-970 (2008).
[5]. Vila, A., Tallman, K.A., Jacobs, A.T., et al. Identification of protein targets of 4-hydroxynonenal using click chemistry for ex vivo biotinylation of azido and alkynyl derivatives. Chemical Research in Toxicology 21(2), 432-444 (2008).
| Cas No. | 82909-47-5 | SDF | |
| 别名 | 13-十四炔酸,13-alkyne Myristic Acid | ||
| 化学名 | 13-tetradecynoic acid | ||
| Canonical SMILES | C#CCCCCCCCCCCCC(O)=O | ||
| 分子式 | C14H24O2 | 分子量 | 224.3 |
| 溶解度 | 10mg/mL in DMSO,10mg/mL in DMF, 12.5mg/mL in Ethanol | 储存条件 | Store at -20°C, protect from light |
| 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 | 4.4583 mL | 22.2916 mL | 44.5831 mL |
| 5 mM | 0.8917 mL | 4.4583 mL | 8.9166 mL |
| 10 mM | 0.4458 mL | 2.2292 mL | 4.4583 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Inhibition of vaccinia virus L1 N-myristoylation by the host N-myristoyltransferase inhibitor IMP-1088 generates non-infectious virions defective in cell entry
PLoS Pathog 2022 Oct 10;18(10):e1010662.PMID:36215331DOI:10.1371/journal.ppat.1010662.
We have recently shown that the replication of rhinovirus, poliovirus and foot-and-mouth disease virus requires the co-translational N-myristoylation of viral proteins by human host cell N-myristoyltransferases (NMTs), and is inhibited by treatment with IMP-1088, an ultrapotent small molecule NMT inhibitor. Here, we examine the importance of N-myristoylation during vaccinia virus (VACV) infection in primate cells and demonstrate the anti-poxviral effects of IMP-1088. N-myristoylated proteins from VACV and the host were metabolically labelled with Myristic Acid Alkyne during infection using quantitative chemical proteomics. We identified VACV proteins A16, G9 and L1 to be N-myristoylated. Treatment with NMT inhibitor IMP-1088 potently abrogated VACV infection, while VACV gene expression, DNA replication, morphogenesis and EV formation remained unaffected. Importantly, we observed that loss of N-myristoylation resulted in greatly reduced infectivity of assembled mature virus particles, characterized by significantly reduced host cell entry and a decline in membrane fusion activity of progeny virus. While the N-myristoylation of VACV entry proteins L1, A16 and G9 was inhibited by IMP-1088, mutational and genetic studies demonstrated that the N-myristoylation of L1 was the most critical for VACV entry. Given the significant genetic identity between VACV, monkeypox virus and variola virus L1 homologs, our data provides a basis for further investigating the role of N-myristoylation in poxviral infections as well as the potential of selective NMT inhibitors like IMP-1088 as broad-spectrum poxvirus inhibitors.