Povilaitis V, Gagnon C, Heisler S
Am J Physiol. 1981 Mar;240(3):G199-205. doi: 10.1152/ajpgi.1981.240.3.G199.
The role of protein carboxyl methylation in amylase secretion from incubated rat pancreatic lobules was assessed. All the components of the carboxyl methylation system, protein carboxyl methylase, methyl-acceptor protein substrates, and protein methylesterase, were found in the rat pancreas. Protein carboxyl methylation is stimulated by both pancreozymin and carbachol at concentrations that are equally effective in stimulating amylase release. The secretagogue-enhanced increase in protein carboxyl methylation was concomitant with the onset of the secretory response. These responses were blocked by the receptor antagonists, dibutyryl cGMP and atropine. Inhibitors of protein carboxyl methylase inhibited carboxyl methylation stimulated by pancreozymin but did not affect the secretory response to the hormone. Ethyleneglycol-bis-(beta-aminoethylether)-N-N'-tetraacetic acid blocked protein carboxyl methylation and amylase release, indicating that extracellular calcium was essential for both processes. The presence or absence of calcium did not alter the enzyme activity in lobule homogenates. The data suggest that only a small part of the total cellular protein carboxyl methylation activity is directly involved in pancreatic enzyme secretion. Like the calcium requirement in secretion, protein carboxyl methylation also lies distal to the stimulant-receptor interaction.
评估了蛋白质羧基甲基化在孵育的大鼠胰腺小叶淀粉酶分泌中的作用。在大鼠胰腺中发现了羧基甲基化系统的所有成分，即蛋白质羧基甲基酶、甲基受体蛋白底物和蛋白质甲酯酶。促胰液素和卡巴胆碱在刺激淀粉酶释放方面具有同等效力的浓度下，均可刺激蛋白质羧基甲基化。促分泌剂增强的蛋白质羧基甲基化增加与分泌反应的开始同时发生。这些反应被受体拮抗剂二丁酰环磷鸟苷和阿托品阻断。蛋白质羧基甲基酶抑制剂抑制促胰液素刺激的羧基甲基化，但不影响对该激素的分泌反应。乙二醇双（β-氨基乙基醚）-N-N'-四乙酸阻断蛋白质羧基甲基化和淀粉酶释放，表明细胞外钙对这两个过程都是必不可少的。有无钙并不改变小叶匀浆中的酶活性。数据表明，细胞总蛋白质羧基甲基化活性中只有一小部分直接参与胰腺酶的分泌。与分泌中对钙的需求一样，蛋白质羧基甲基化也位于刺激物-受体相互作用的下游。
