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Acyl-CoA

About: Acyl-CoA is a research topic. Over the lifetime, 527 publications have been published within this topic receiving 25134 citations. The topic is also known as: Acyl Coenzyme A.


Papers
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Journal ArticleDOI
TL;DR: It is concluded that the chain-shortened epoxy-fatty acids are produced primarily by peroxisomal beta-oxidation, and may serve as an alternate mechanism for EET inactivation and removal from the tissues.

36 citations

Journal ArticleDOI
TL;DR: It seems very likely that CoA-mediated cleavage of phospholipids/ATP-independent acyl-CoA synthesis is implicated in the metabolism of certain types of fatty acyl residues of membranous phospholIPids in mammalian cells.

36 citations

Journal ArticleDOI
TL;DR: There appears to be some consensus in the amino acid sequence for acyl CoA binding sites on these proteins which serve a variety of important roles in cellular metabolism.
Abstract: Long chain fatty acyl CoA esters have the ability to interact with certain proteins and thereby serve as effectors in cell metabolism. In particular, they can displace nucleotides from specific nucleotide dependent or binding proteins and interfere with their action. The ADP/ATP carrier and uncoupling protein are two examples where the interplay of nucleotide and acyl CoA binding to the proteins regulate their function. Other proteins such as glucokinase can be considered in this group. In certain tissues like liver they are affected during fasting and insulin deficiency, and when serum fatty acids and liver acyl CoA levels are elevated. More recently, an acyl CoA binding protein in E. coli has been found to be a transcription factor for gene regulation of fatty acid metabolism enzymes. There appears to be some consensus in the amino acid sequence for acyl CoA binding sites on these proteins which serve a variety of important roles in cellular metabolism.

36 citations

Journal ArticleDOI
TL;DR: The inhibition of neutral TG lipase activity by fatty acyl CoA is consistent with the observation that metabolic interventions that increase tissue levels of fatty acol CoA result in an inhibition of rates of cardiac lipolysis.

36 citations

Journal ArticleDOI
TL;DR: The data demonstrate that elevation of H2O2 formation by acyl CoA oxidase activity measured in vitro is not necessarily associated with increases in rates of H 2O2 generation in intact perfused liver or in vivo, most likely due to rate-limitation in intact cells by fatty acid supply.

36 citations


Network Information
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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20232
202212
20218
20205
20193
20185