Alemany S, Varela I, Harper J F, Mato J M
J Biol Chem. 1982 Aug 25;257(16):9249-51.
The addition of micromolar Ca2+ in the presence of ATP (10 microM) to rat liver microsomes stimulates phospholipid methylation and the formation of fatty acid methyl esters. Our data indicate that calmodulin mediates the effect of Ca2+ on both phospholipid and fatty acid methylation. This evidence includes: 1) chlorpromazine, an inhibitor of Ca2+ effects mediated through calmodulin, prevented the activation by Ca2+ plus ATP of the methylation reactions; 2) isolation of the microsomes in the presence of ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (5 mM), to remove endogenous calmodulin also prevented Ca2+ plus ATP stimulation of both phospholipid and fatty acid methylation; 3) the addition of exogenous calmodulin to microsomes isolated in the presence of 5 mM ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid restored Ca3+ plus ATP stimulation of both classes of lipids: and 4) pre-incubation of liver microsomes with an antiserum against calmodulin prevented the activation of lipid methylation by Ca2+ plus ATP.
在ATP（10微摩尔）存在的情况下，向大鼠肝脏微粒体中添加微摩尔浓度的Ca2+会刺激磷脂甲基化以及脂肪酸甲酯的形成。我们的数据表明，钙调蛋白介导了Ca2+对磷脂和脂肪酸甲基化的作用。这些证据包括：1）氯丙嗪是通过钙调蛋白介导的Ca2+效应的抑制剂，它能阻止Ca2+加ATP对甲基化反应的激活；2）在乙二醇双（β-氨基乙基醚）-N，N，N'，N'-四乙酸（5毫摩尔）存在的情况下分离微粒体以去除内源性钙调蛋白，也能阻止Ca2+加ATP对磷脂和脂肪酸甲基化的刺激；3）向在5毫摩尔乙二醇双（β-氨基乙基醚）-N，N，N'，N'-四乙酸存在下分离得到的微粒体中添加外源性钙调蛋白，可恢复Ca3+加ATP对这两类脂质的刺激；4）用抗钙调蛋白抗血清对肝脏微粒体进行预孵育可阻止Ca2+加ATP对脂质甲基化的激活。
