Topic
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 published on a yearly basis
Papers
More filters
TL;DR: β 3 -adrenoceptor agonists have a more rapid insulin-sensitising than anti-obesity effect, possibly because stimulation of lipid oxidation rapidly lowers intracellular long-chain fatty acyl CoA and diacylglycerol levels, which may deactivate those protein kinase C isoenzymes that inhibit insulin signalling.
197 citations
TL;DR: In this paper, the authors identify enzymes that remove N-terminal myristoyl-glycine or myristate from lysines, and these enzymes are potential drug targets in human diseases.
197 citations
TL;DR: Evidence from directed experimentation, as well as information obtained by mining the molecular biological databases suggesting the long chain ACS enzymes are required in protein acylation, vesicular trafficking, signal transduction pathways and cell wall synthesis are presented.
191 citations
TL;DR: The concentrations of lysophosphatidylcholine, which are higher in atherosclerotic than in control aortic tissues, could be a factor controlling rates of fatty acid incorporation into phosphatidylethanolamine.
180 citations
TL;DR: The results suggest that long-chain acyl-CoA esters synthesized for either triacylglycerol synthesis or beta-oxidation have to pass through the acyl -CoA/ACBP pool before utilization, and ACBP has a duel function in creating a cytosolic pool of acyl
Abstract: It is shown that acyl-CoA binding protein (ACBP), in contrast with fatty acid binding protein (FABP), stimulates the synthesis of long-chain acyl-CoA esters by mitochondria. ACBP effectively opposes the product feedback inhibition of the long-chain acyl-CoA synthetase by sequestration of the synthesized acyl-CoA esters. Feedback inhibition of microsomal long-chain acyl-CoA synthesis could not be observed, due to the formation of small acyl-CoA binding vesicles during preparation and/or incubation. Microsomal membrane preparations are therefore unsuitable for studying feedback inhibition of long-chain acyl-CoA synthesis. ACBP was found to have a strong attenuating effect on the long-chain acyl-CoA inhibition of both acetyl-CoA carboxylase and mitochondrial adenine nucleotide translocase. Both processes were unaffected by the presence of long-chain acyl-CoA esters when the ratio of long-chain acyl-CoA to ACBP was below 1, independent of the acyl-CoA concentration used. It is therefore not the acyl-CoA concentration as such which is important from a regulatory point of view, but the ratio of acyl-CoA to ACBP. The cytosolic ratio of long-chain acyl-CoA to ACBP was shown to be well below 1 in the liver of fed rats. ACBP could compete with the triacylglycerol-synthesizing pathway, but not with the phospholipid-synthesizing enzymes, for acyl-CoA esters. Furthermore, in contrast with FABP, ACBP was able to protect long-chain acyl-CoA esters against hydrolysis by microsomal acyl-CoA hydrolases. The results suggest that long-chain acyl-CoA esters synthesized for either triacylglycerol synthesis or beta-oxidation have to pass through the acyl-CoA/ACBP pool before utilization. This means that acyl-CoA synthesized by microsomal or mitochondrial synthetases is uniformly available in the cell. It is suggested that ACBP has a duel function in (1) creating a cytosolic pool of acyl-CoA protected against acyl-CoA hydrolases, and (2) protecting vital cellular processes from being affected by long-chain acyl-CoA esters.
179 citations