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Merck

C3019

Sigma-Aldrich

辅酶 A 三锂盐

≥93%

别名:

CoA Li3

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About This Item

经验公式(希尔记法):
C21H33Li3N7O16P3S
CAS号:
分子量:
785.33
EC號碼:
MDL號碼:
分類程式碼代碼:
41106305
PubChem物質ID:
NACRES:
NA.51

品質等級

化驗

≥93%

形狀

powder

儲存溫度

−20°C

SMILES 字串

[Li+].[Li+].[Li+].CC(C)(COP([O-])(=O)OP([O-])(=O)OC[C@H]1O[C@H]([C@H](O)[C@@H]1OP(O)([O-])=O)n2cnc3c(N)ncnc23)C(O)C(=O)NCCC(=O)NCCS

InChI

1S/C21H36N7O16P3S.3Li/c1-21(2,16(31)19(32)24-4-3-12(29)23-5-6-48)8-41-47(38,39)44-46(36,37)40-7-11-15(43-45(33,34)35)14(30)20(42-11)28-10-27-13-17(22)25-9-26-18(13)28;;;/h9-11,14-16,20,30-31,48H,3-8H2,1-2H3,(H,23,29)(H,24,32)(H,36,37)(H,38,39)(H2,22,25,26)(H2,33,34,35);;;/q;3*+1/p-3/t11-,14-,15-,16?,20-;;;/m1.../s1

InChI 密鑰

QSCBPHBAFBVXRK-HJKJOZROSA-K

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一般說明

辅酶A(CoA)由磷酸泛酸酯在泛酸激酶的作用下合成,是主要的调节剂。

應用

辅酶A三锂盐用于:
  • 生成乙酰转移酶Gcn5酰化动力学分析的标准曲线
  • 作为 JNADH 和 JNADPH 生产分析中的辅助因子
  • 标记 Alexa647(AF647)探针

生化/生理作用

辅酶 A(CoA、CoASH、HSCoA)是促进酶促酰基转移反应,并支持脂肪酸合成和氧化的辅酶。CoA 参与多种酶的作用机制。酰基辅酶 A 积累与代谢紊乱有关,可能间接导致与碳诱导线粒体应激性心力衰竭、糖尿病和肥胖症相关的发病机制。

其他說明

有关更多技术信息和辅酶 A 衍生物的完整列表,请访问酰基转移试剂资源

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, type N95 (US)


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Structural basis for acyl-group discrimination by human Gcn5L2
Ringel AE and Wolberger C
Acta crystallographica. Section D, Structural biology, 72(7), 841-848 (2016)
Constructing a synthetic pathway for acetyl-coenzyme A from one-carbon through enzyme design
Lu X, et al.
Nature Communications, 10(1), 1378-1378 (2019)
Pantothenate kinase regulation of the intracellular concentration of coenzyme A
Rock CO, et al.
The Journal of biological chemistry, 275(2), 1377-1383 (2000)
Respiratory phenomics across multiple models of protein hyperacylation in cardiac mitochondria reveals a marginal impact on bioenergetics
Fisher-Wellman KH, et al.
Cell Reports, 26(6), 1557-1572 (2019)
Jessica P Kuppan et al.
eLife, 10 (2021-09-30)
The complement system is a critical host defense against infection, playing a protective role that can also enhance disease if dysregulated. Although many consequences of complement activation during viral infection are well established, mechanisms that determine the extent to which

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