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编 号：F318583
分子式：C23H38N7O17P3S
分子量：809.57
分子式：C23H38N7O17P3S
分子量：809.57
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CAS No: 32140-51-5
产品详情
生物活性：
Acetyl-coenzyme A (Acetyl-CoA) lithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A lithium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A lithium is also a key precursor of lipid synthesis.
体内研究：
Acetyl coenzyme A lithium blunts pressure overload-induced cardiomyopathy in a mice cardiac pressure overload model by Suppressing maladaptive autophagy.Mice deprived of food (but with access to water ad libitum) for 24 h exhibit a significant reduction in total Acetyl coenzyme A lithium levels in several organs, including the heart and muscles, corresponding to a decrease in protein acetylation levels. However, the same experimental conditions have no major effects on Acetyl coenzyme A lithium concentrations in the brain and actually increase hepatic Acetyl coenzyme A lithium and protein acetylation levels.
体外研究：
Acetyl coenzyme A lithium increases cytoplasmic protein acetylation in starved U2OS cells while reducing starvation-induced autophagic fluxes. (U2OS cells stably expressing GFP-LC3 and are microinjected with Acetyl coenzyme A lithium; incubated in nutrient-free conditions in the presence of 100 nM BafA1 and fixed after 3 h).
Acetyl-coenzyme A (Acetyl-CoA) lithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A lithium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A lithium is also a key precursor of lipid synthesis.
体内研究：
Acetyl coenzyme A lithium blunts pressure overload-induced cardiomyopathy in a mice cardiac pressure overload model by Suppressing maladaptive autophagy.Mice deprived of food (but with access to water ad libitum) for 24 h exhibit a significant reduction in total Acetyl coenzyme A lithium levels in several organs, including the heart and muscles, corresponding to a decrease in protein acetylation levels. However, the same experimental conditions have no major effects on Acetyl coenzyme A lithium concentrations in the brain and actually increase hepatic Acetyl coenzyme A lithium and protein acetylation levels.
体外研究：
Acetyl coenzyme A lithium increases cytoplasmic protein acetylation in starved U2OS cells while reducing starvation-induced autophagic fluxes. (U2OS cells stably expressing GFP-LC3 and are microinjected with Acetyl coenzyme A lithium; incubated in nutrient-free conditions in the presence of 100 nM BafA1 and fixed after 3 h).
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