Coenzyme A (lithium salt)
(Synonyms: 辅酶A三锂盐) 目录号 : GC43294
辅酶 A（锂盐）是一种普遍存在的必需辅因子，是柠檬酸循环和脂肪酸代谢的酰基载体和羰基活化基团。
Cas No.:18439-24-2
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
Coenzyme A (CoA) is an essential cofactor functioning as an acyl group carrier and carbonyl-activating group for the citric acid cycle and fatty acid metabolism. About 4% of cellular enzymes utilize CoA as a substrate. It is synthesized from pantothenic acid in a five-step process that requires ATP. The pantothenate kinase step of the CoA biosynthetic pathway has been identified as a target for the development of antibacterial compounds.
| Cas No. | 18439-24-2 | SDF | |
| 别名 | 辅酶A三锂盐 | ||
| Canonical SMILES | O[C@H]1[C@H](N2C=NC3=C2N=CN=C3N)O[C@H](COP(OP(OCC(C)(C)[C@@H](O)C(NCCC(NCCS)=O)=O)([O-])=O)([O-])=O)[C@H]1OP([O-])(O)=O.[Li+].[Li+].[Li+] | ||
| 分子式 | C21H33N7O16P3S•3Li | 分子量 | 785.3 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.2734 mL | 6.367 mL | 12.734 mL |
| 5 mM | 0.2547 mL | 1.2734 mL | 2.5468 mL |
| 10 mM | 0.1273 mL | 0.6367 mL | 1.2734 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。
Short communication: indigestible markers reduce the mammary Delta9-desaturase index and alter the milk fatty acid composition in cows
J Dairy Sci 2006 Aug;89(8):3006-10.PMID:16840616DOI:10.3168/jds.S0022-0302(06)72573-5.
Accurate determination of the flow of nutrients at the omasum requires the use of a triple marker system. Typically, a system based on ruminal administration of the lithium salt of CoEDTA, ytterbium acetate (Yb-Ac), and chromium-mordanted straw (Cr-S) has been used. However, there is evidence to suggest that product:substrate ratios for stearoyl-coenzyme A desaturase (Delta(9)-desaturase) are lower in milk fat from cows administered a combination of CoEDTA, Yb-Ac, and Cr-S, indicating reduced Delta(9)-desaturase activity. To evaluate this hypothesis, samples of milk were collected 1 d before, and on d 2, 6, and 9 of administering the CoEDTA, Yb-Ac, and Cr-S triple marker system into the rumen of 4 cows. A 4 x 4 Latin square with 28-d experimental periods was used to assess the effects of 0, 75, 150, and 300 g/d of fish oil in the diet on ruminal and mammary lipid metabolism. Irrespective of the amount of fish oil in the diet, concentrations of all milk fatty acids containing a cis-9 double bond were reduced after markers were given. Milk fatty acid pairs dependent on Delta(9)-desaturase were decreased over time, with responses reaching a nadir within 6 d of marker administration. Overall, administering markers into the rumen was associated with a mean decrease in milk cis-9 10:1/ 10:0, cis-9 12:1/12:0, cis-9 14:1/14:0, cis-9 16:1/16:0, cis-9 17:1/17:0, cis-9 18:1/18:0, and cis-9,trans-11 conjugated linoleic acid/trans-11 18:1 concentration ratios of 44.6, 52.7, 58.7, 36.8, 37.2, 44.3, and 43.0%, respectively. In conclusion, one or more of the markers administered altered milk fatty acid composition and may act as an inhibitor of Delta(9)-desaturase in the bovine mammary gland.
Overexpression of NtHAL3 genes confers increased levels of proline biosynthesis and the enhancement of salt tolerance in cultured tobacco cells
J Exp Bot 2004 Feb;55(396):387-95.PMID:14739262DOI:10.1093/jxb/erh043.
The Hal3 protein of Saccharomyces cerevisiae inhibits the activity of PPZ1 type-1 protein phosphatases and functions as a regulator of salt tolerance and cell cycle control. In plants, two HAL3 homologue genes in Arabidopsis thaliana, AtHAL3a and AtHAl3b, have been isolated and the function of AtHAL3a has been investigated through the use of transgenic plants. Expressions of both AtHAL3 genes are induced by salt stress. AtHAL3a overexpressing transgenic plants exhibit improved salt and sorbitol tolerance. In vitro studies have demonstrated that AtHAL3 protein possessed 4'-phosphopantothenoylcysteine decarboxylase activity. This result suggests that the molecular function of plant HAL3 genes is different from that of yeast HAL3. To understand the function of plant HAL3 genes in salt tolerance more clearly, three tobacco HAL3 genes, NtHAL3a, NtHAL3b, and NtHAL3c, from Nicotiana tabacum were identified. NtHAL3 genes were constitutively expressed in all organs and under all conditions of stress examined. Overexpression of NtHAL3a improved salt, osmotic, and lithium tolerance in cultured tobacco cells. NtHAL3 genes could complement the temperature-sensitive mutation in the E. coli dfp gene encoding 4'-phosphopantothenoyl-cysteine decarboxylase in the Coenzyme A biosynthetic pathway. Cells overexpressing NtHAL3a had an increased intracellular ratio of proline. Taken together, these results suggest that NtHAL3 proteins are involved in the Coenzyme A biosynthetic pathway in tobacco cells.
Pravastatin has no direct effect on transmembrane cationic transport systems in human erythrocytes and platelets
Eur J Clin Pharmacol 1994;47(3):281-3.PMID:7867682DOI:10.1007/BF02570509.
In vitro incubation of human erythrocytes and platelets with the 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitor pravastatin in the concentration range 1 nM to 10 microM did not affect the activity of the Na(+)-K(+)-pump, Na(+)-K(+)-cotransport or Na(+)-Li(+)-countertransport, or the ground membrane leak for Na+ and K+. The data indicate that pravastatin has no direct effect on transmembrane cationic transport systems in red blood cells or platelets.