Cameron C M, Rillema J A
Endocrinology. 1983 Nov;113(5):1596-600. doi: 10.1210/endo-113-5-1596.
The depletion of extracellular calcium ions by EGTA abolishes the PRL stimulation of [14C]acetate incorporation into lipids in mouse mammary gland explants. This abolition is reversed by the addition of calcium, but not magnesium. The chelation of calcium ions was similarly shown in earlier studies to abolish PRL's actions on RNA and casein synthesis. When the actions of PRL on lipid, RNA, and casein biosynthesis were tested when the extracellular calcium ion concentration was varied, it was observed that 5-10 microM calcium was required for PRL to manifest its actions. The calcium ionophore A23187 was unable, however, to mimic the PRL stimulation of lipid, RNA, or casein synthesis. Trifluoperazine, an inhibitor of calmodulin action had no effect on the PRL-induced synthesis of lipids, RNA, or casein, except at pharmacological levels.
乙二醇双四乙酸（EGTA）使细胞外钙离子耗竭，从而消除了催乳素（PRL）对小鼠乳腺外植体中[14C]乙酸掺入脂质的刺激作用。添加钙可逆转这种消除作用，但添加镁则不能。早期研究同样表明，钙离子螯合可消除PRL对RNA和酪蛋白合成的作用。当细胞外钙离子浓度变化时，测试PRL对脂质、RNA和酪蛋白生物合成的作用，发现PRL发挥其作用需要5-10微摩尔的钙。然而，钙离子载体A23187无法模拟PRL对脂质、RNA或酪蛋白合成的刺激作用。除了在药理剂量下，钙调蛋白作用抑制剂三氟拉嗪对PRL诱导的脂质、RNA或酪蛋白合成没有影响。
