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Merck
CN

K1502

α-酮戊二酸脱氢酶 来源于猪心脏

buffered aqueous glycerol solution, 0.1-1.0 units/mg protein (Lowry)

别名:

多酶2-氧戊二酸脱氢酶配合物

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关于此项目

化学文摘社编号:
UNSPSC Code:
12352204
NACRES:
NA.54
MDL number:
Specific activity:
0.1-1.0 units/mg protein (Lowry)
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产品名称

α-酮戊二酸脱氢酶 来源于猪心脏, buffered aqueous glycerol solution, 0.1-1.0 units/mg protein (Lowry)

form

buffered aqueous glycerol solution

specific activity

0.1-1.0 units/mg protein (Lowry)

foreign activity

pyruvate dehydrogenase ≤20%

shipped in

dry ice

storage temp.

−20°C

Quality Level

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Analysis Note

可能含有痕量的聚乙二醇。

Application

α猪心α-酮戊二酸脱氢酶已用于:
  • 研究过氧亚硝酸盐处理细胞中谷胱甘肽(GSH)的反硝化作用
  • 通过Spectramax M5微孔板分光荧光计检测其在心肌线粒体中的活性
  • 作为阳性对照,通过Spectramax GEMINI EM荧光微孔板读板机评估其在小鼠神经元中的活性

Biochem/physiol Actions

αα-酮戊二酸脱氢酶(α-KGDH)是生物能量学过程的关键酶,是Krebs循环或三羧酸(TCA)循环代谢流的调控物。它通过还原型烟酰胺腺嘌呤二核苷酸(NADH)的释放,催化α-酮戊二酸氧化脱羧为琥珀酰-CoA。这是TCA循环中的限速反应。该反应为呼吸链提供电子,需要硫胺素焦磷酸作为辅因子。反应速率由NAD(烟酰胺腺嘌呤二核苷酸)还原决定。αα-KGDH的最佳pH值范围为6.6-7.4。该酶会被氧化应激抑制并导致代谢缺乏。但α-KGDH又能产生活性氧(ROS)导致氧化应激。α-KGDH缺陷或浓度不够会导致好几种神经退行性疾病,比如阿尔茨海默病。
α-酮戊二酸脱氢酶对肿瘤微环境改变的反应最灵敏,与癌症的适应性代谢反应有关。抑制α-酮戊二酸脱氢酶可对抗乳腺癌相关的肺转移。

General description

研究领域:Neuroscience

α-酮戊二酸脱氢酶(α-KGDH)是位于线粒体的一种多酶复合体。这种复合酶由多个单位的硫胺素焦磷酸依赖性脱氢酶(E1)、二氢硫辛酰脱氢酶(E3)和二氢硫辛酰转琥珀酰酶(E2)组成。

Other Notes

在 30 °C、pH 7.4、饱和水平的辅酶 A 存在的条件下,一单位每分钟可将 1.0 μ 摩尔的 β-NAD 转化成 β-NADH。

Physical form

以 50% 甘油溶液的形式提供,含有 9mg 每毫升的牛血清白蛋白、30% 蔗糖、1.5 mM EDTA、1.5 mM EGTA、1.5 mM 2-巯基乙醇、0.3% TRITON X-100、0.003% 叠氮化钠和 15 mM 磷酸钾,pH 6.8。

Legal Information

Triton is a trademark of The Dow Chemical Company or an affiliated company of Dow

hcodes

Hazard Classifications

Aquatic Chronic 3

存储类别

10 - Combustible liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

法规信息

含少量动物源组分生物产品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Lidan Sun et al.
Journal of neurochemistry, 158(2), 282-296 (2021-04-28)
Metabolic changes that correlate to cognitive changes are well-known in Alzheimer's disease (AD). Metabolism is often linked to functional changes in proteins by post-translational modifications. The importance of the regulation of transcription by acetylation is well documented. Advanced mass spectrometry
Ana Cristina Roginski et al.
Biochimica et biophysica acta. Molecular basis of disease, 1866(5), 165682-165682 (2020-01-14)
Propionic acidemia is caused by lack of propionyl-CoA carboxylase activity. It is biochemically characterized by accumulation of propionic (PA) and 3-hydroxypropionic (3OHPA) acids and clinically by severe encephalopathy and cardiomyopathy. High urinary excretion of maleic acid (MA) and 2-methylcitric acid
Laszlo Tretter et al.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 360(1464), 2335-2345 (2005-12-03)
Alpha-ketoglutarate dehydrogenase (alpha-KGDH) is a highly regulated enzyme, which could determine the metabolic flux through the Krebs cycle. It catalyses the conversion of alpha-ketoglutarate to succinyl-CoA and produces NADH directly providing electrons for the respiratory chain. alpha-KGDH is sensitive to
Wagner L Araújo et al.
The Plant cell, 24(6), 2328-2351 (2012-07-04)
Transgenic tomato (Solanum lycopersicum) plants expressing a fragment of the gene encoding the E1 subunit of the 2-oxoglutarate dehydrogenase complex in the antisense orientation and exhibiting substantial reductions in the activity of this enzyme exhibit a considerably reduced rate of
Qingli Shi et al.
The Journal of biological chemistry, 286(20), 17640-17648 (2011-04-02)
Reduced brain metabolism is an invariant feature of Alzheimer Disease (AD) that is highly correlated to the decline in brain functions. Decreased activities of key tricarboxylic acid cycle (TCA) cycle enzymes may underlie this abnormality and are highly correlated to

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