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CA2 — COA3

Text-mined interactions from Literome

Siliprandi et al., Mol Cell Biochem 1992 : The dissipation of membrane potential by low concentrations of palmitoyl CoA in the presence of Ca2+ , but not that of high concentrations of palmitoyl CoA alone, was prevented by either ruthenium red, Cyclosporin A or Mg2+, but reversed only by Mg2+
Berge et al., Scand J Clin Lab Invest 1978 : Mg2+, Mn2+, Ca2+ and Triton X-100 inhibited the palmitoyl-CoA hydrolase activity
Boquist et al., Cell Calcium 1986 : The release of accumulated Ca2+ was stimulated by arsenite, malonate, PMB, palmitoyl-CoA and succinyl-CoA, whereas the release was inhibited by dibucaine, fluorocitrate, trifluoroperazine, and by oligomycin, especially in the presence of ADP
Wolkowicz et al., J Biol Chem 1980 : However, when mitochondria accumulate Ca2+ in the presence of lactate, neither acetoacetate nor palmitoyl-CoA addition results in Ca2+ release and no swelling is observed
Rich et al., Biochem J 1995 : ( 3 ) Under conditions where acyl-CoA binding is inhibited, CoA causes increased Ca2+ accumulation, apparently by decreasing the Ca2+ leak rate
Rys-Sikora et al., J Biol Chem 1994 : Using permeabilized DDT1MF-2 smooth muscle cells, 2 microM palmitoyl-CoA completely blocked Ca2+ release activated by 20 microM GTP, while having no effect on inositol 1,4,5-trisphosphate induced Ca2+ release ... In contrast, 10 microM CoA itself blocked GTP induced Ca2+ release ... In the presence of oxalate, GTP activated Ca2+ transfer results in a substantial increase in Ca2+ accumulation ; palmitoyl-CoA also completely reversed this effect resulting in rapid termination of Ca2+ uptake
Comerford et al., Biochem J 1993 : Effects of CoA and acyl-CoAs on GTP dependent Ca2+ release and vesicle fusion in rat liver microsomal vesicles ... By investigation of the effects of CoA and palmitoyl-CoA on the thapsigargin induced passive leak rate of Ca2+, and on the latency of the mannose-6-phosphatase of the vesicles, we conclude that CoA and palmitoyl-CoA cause decreased vesicle permeability rather than stimulation of Ca2+ pumping activity
Chini et al., Am J Physiol 1996 : Palmitoyl-CoA induced Ca2+ release was suppressed by ruthenium red, spermine, and the calmodulin antagonist N- ( 6-aminohexyl ) -1-naphthalenesulfonamide, which all prevent activation of the ryanodine channel, but not by heparin or thionicotinamide-NADP ... In addition, cADPR was able to desensitize the sea urchin egg homogenates to the subsequent Ca2+ release induced by palmitoyl-CoA and vice versa ... We propose that palmitoyl-CoA , present in micromolar concentrations, may trigger Ca2+ release through the ryanodine channel and, in lower concentrations, may increase the sensitivity of the Ca2+ release system to cADPR
Bauldry et al., Biochim Biophys Acta 1996 : Removal of acetyl CoA from the system had little effect on LTB4 generation but blocked PAF production with a concomitant increase in lyso-PAF formation LTB4 and PAF production occurred in parallel over time and at differing ATP and Ca2+ concentrations