75520-41-1

75520-41-1 structure
75520-41-1 structure
  • Name: Acetyl coenzyme A trilithium
  • Chemical Name: Acetyl coenzyme A trilithium salt
  • CAS Number: 75520-41-1
  • Molecular Formula: C23H35Li3N7O17P3S
  • Molecular Weight: 827.370
  • Catalog: Signaling Pathways Autophagy Autophagy
  • Create Date: 2018-08-21 16:02:38
  • Modify Date: 2024-01-10 20:22:21
  • 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].

Name Acetyl coenzyme A trilithium salt
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].
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

[1]. Choudhary C, et al. The growing landscape of lysine acetylation links metabolism and cell signalling. Nat Rev Mol Cell Biol. 2014 Aug;15(8):536-50.  

[2]. Mariño G, et al. Regulation of autophagy by cytosolic acetyl-coenzyme A. Mol Cell. 2014 Mar 6;53(5):710-25.  

[3]. Zhu H, et al. Cardiac autophagy is a maladaptive response to hemodynamic stress. J Clin Invest. 2007 Jul;117(7):1782-93.  

[4]. Pietrocola F, et al. Acetyl coenzyme A: a central metabolite and second messenger. Cell Metab. 2015 Jun 2;21(6):805-21.  

Molecular Formula C23H35Li3N7O17P3S
Molecular Weight 827.370
Exact Mass 827.150330
PSA 421.19000
LogP 0.48580
Hazard Codes Xi:Irritant;
Risk Phrases R36/37/38
Safety Phrases S26-S36/37