High impact information on CPD-18

• The recombinant ALCAT1 enzyme recognizes both monolysocardiolipin and dilysocardiolipin as substrates with a preference for linoleoyl-CoA and oleoyl-CoA as acyl donors [1].
• We confirm by using a similar experimental approach that, in contrast, the human Delta 6-desaturase uses linoleoyl-CoA as substrate, which results in high efficiency of the subsequent elongation step [2].
• Lauroyl-CoA, myristoyl-CoA, and palmitoyl-CoA were good substrates for elongation by isolated microsomes; oleoyl-CoA, and linoleoyl-CoA were intermediate; and stearoyl-CoA was a very poor substrate [3].
• The intramembrane localization of linoleoyl-CoA desaturase in rat liver microsomes was examined by various methods, such as digestion by proteases, effect of detergents, and inhibition by the antibodies against purified terminal desaturase [4].
• SZ-induced diabetes also increased acyl-CoA;1-acylglycerol 3-phosphorylcholine acyltransferase (GPCAT) activity (38-45 per cent, p less than 0.01) with 3 different acyl-CoA donors: oleoyl-CoA, linoleoyl-CoA and arachidonoyl-CoA [5].

Biological context of CPD-18

• Moreover, palmitoyl-CoA and linoleoyl-CoA served equally well as the acyl donor for the acylation reaction [6].

Anatomical context of CPD-18

• Cytoplasmic location of linoleoyl-CoA desaturase in microsomal membranes of rat liver [4].
• Control levels of myristoyl-, palmitoyl-, stearoyl-, arachidonoyl-, oleoyl- and linoleoyl-CoA were 0.6, 3.2, 4.7, 3.4, 2.4 and 3.0 micrograms/uterus and were increased 39, 110, 146, 100, 84 and 69% at 36-48 h, respectively [7].
• The effect of linoleoyl CoA was specific for Ca2+ transport; sodium-dependent phosphate uptake was slightly inhibited and the activity of alkaline phosphatase, a brush-border enzyme, was unaffected [8].
• Lysophosphatidylinositol acyltransferase utilizing arachidonoyl CoA and lysophosphatidylcholine acyltransferase utilizing linoleoyl CoA were measured in subcellular fractions of rat brain [9].

Associations of CPD-18 with other chemical compounds

• An increase in the percentage of monoenoic fatty acids and a decrease in the n-6 acid family in liver phospholipids, linoleoyl-CoA desaturase, and PGE(2) synthase activities in liver microsomes were observed in ethanol-treated rats [10].

References