抗原诱导肥大细胞质膜中蛋白激酶C活性增加。
Antigen-induced increase in protein kinase C activity in plasma membrane of mast cells.
作者信息
White J R, Pluznik D H, Ishizaka K, Ishizaka T
出版信息
Proc Natl Acad Sci U S A. 1985 Dec;82(23):8193-7. doi: 10.1073/pnas.82.23.8193.
Bridging of cell-bound IgE antibody molecules on colony-stimulating factor-dependent mouse mast cell line (PT-18) cells by multivalent antigen induces phospholipid methylation, a transient rise in intracellular cAMP, intracellular mobilization and uptake of Ca2+, and formation of diacylglycerol followed by histamine release. Exposure of the sensitized cells to antigen also induces a substantial increase in protein kinase C activity in the plasma membrane, which is accompanied by a slight decrease in the enzyme in cytosol. Protein kinase C activity in the membrane fraction reached maximum within 30 sec after antigen challenge and then gradually declined. The increase of the enzyme activity in the membrane could not be explained by a shift of the enzyme from cytosol, and it suggested that bridging of IgE-receptor may induce a modulation of existing enzyme to a state of higher catalytic activity. Phorbol 12-myristate 13-acetate also induced a rapid but persistent increase in protein kinase C activity in the membrane fraction of mast cells. However, the increase in the enzyme activity in the membrane was accompanied by a marked decrease in the enzyme in cytosol.
多价抗原使集落刺激因子依赖性小鼠肥大细胞系（PT-18）细胞上结合细胞的IgE抗体分子桥联，可诱导磷脂甲基化、细胞内cAMP短暂升高、细胞内Ca2+动员与摄取、二酰基甘油形成，随后组胺释放。致敏细胞暴露于抗原还可诱导质膜中蛋白激酶C活性大幅增加，同时胞质溶胶中该酶略有下降。抗原攻击后30秒内，膜组分中的蛋白激酶C活性达到最大值，然后逐渐下降。膜中酶活性的增加无法用酶从胞质溶胶的转移来解释，这表明IgE受体桥联可能诱导现有酶调节至更高催化活性状态。佛波酯12-肉豆蔻酸酯13-乙酸酯也可诱导肥大细胞膜组分中蛋白激酶C活性快速但持续增加。然而，膜中酶活性的增加伴随着胞质溶胶中酶的显著下降。
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