1. Others Metabolic Enzyme/Protease Autophagy
  2. Oxidative Phosphorylation Endogenous Metabolite Autophagy
  3. Acetyl coenzyme A trilithium

Acetyl coenzyme A trilithium  (Synonyms: Acetyl-CoA trilithium)

Cat. No.: HY-114293A
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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.

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Acetyl coenzyme A trilithium Chemical Structure

Acetyl coenzyme A trilithium Chemical Structure

CAS No. : 75520-41-1

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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].

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial
Molecular Weight

827.37

Formula

C23H35Li3N7O17P3S

CAS No.
SMILES

O[C@H]1[C@@H](O[C@H](COP(OP(OCC(C)([C@H](O)C(NCCC(NCCSC(C)=O)=O)=O)C)(O[Li])=O)(O[Li])=O)[C@H]1OP(O)(O[Li])=O)N2C3=C(C(N)=NC=N3)N=C2

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Room temperature in continental US; may vary elsewhere.

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Acetyl coenzyme A trilithium
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