Name | Acetyl coenzyme A trilithium salt |
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Synonyms |
Adenosine, 5'-O-[[[[(3R)-4-[[3-[[2-(acetylthio)ethyl]amino]-3-oxopropyl]amino]-3-hydroxy-2,2-dimethyl-4-oxobutoxy]hydroxyphosphinyl]oxy]hydroxyphosphinyl]-, 3'-(dihydrogen phosphate), lithium salt (1:3)
acetyl coenzyme a trilithium salt |
Description | Acetyl-coenzyme A (Acetyl-CoA) trilithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A trilithium 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 trilithium is also a key precursor of lipid synthesis[1][2][3][4]. |
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Related Catalog | |
In Vitro | Acetyl coenzyme A trilithium 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; incubated in nutrient-free conditions in the presence of 100 nM BafA1 and fixed after 3 h)[2]. |
In Vivo | Acetyl coenzyme A trilithium blunts pressure overload-induced cardiomyopathy in a mice cardiac pressure overload model by Suppressing maladaptive autophagy[2][3].Mice deprived of food (but with access to water ad libitum) for 24 h exhibit a significant reduction in total Acetyl coenzyme A 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 concentrations in the brain and actually increase hepatic Acetyl coenzyme A and protein acetylation levels[4]. |
References |
Molecular Formula | C23H35Li3N7O17P3S |
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Molecular Weight | 827.370 |
Exact Mass | 827.150330 |
PSA | 421.19000 |
LogP | 0.48580 |
Hazard Codes | Xi:Irritant; |
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Risk Phrases | R36/37/38 |
Safety Phrases | S26-S36/37 |