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

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

Cat. No.: HY-113596A Purity: 97%
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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.

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Acetyl coenzyme A lithium Chemical Structure

Acetyl coenzyme A lithium Chemical Structure

CAS No. : 32140-51-5

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Based on 2 publication(s) in Google Scholar

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2 Publications Citing Use of MCE Acetyl coenzyme A lithium

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Description

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[1][2][3][4].

IC50 & Target

Human Endogenous Metabolite

 

In Vitro

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)[2].

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

In Vivo

Acetyl coenzyme A lithium 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 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[4].

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

Clinical Trial
Molecular Weight

809.57

Formula

C23H38N7O17P3S

CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=P(OCC([C@@H](O)C(NCCC(NCCSC(C)=O)=O)=O)(C)C)(O)OP(OC[C@@H]1[C@@H](OP(O)(O)=O)[C@@H](O)[C@H](N2C3=NC=NC(N)=C3N=C2)O1)(O)=O.[xLi]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Purity & Documentation
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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 lithium
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