蛋白激酶C激活剂通过阻止小窝内吞作用来抑制受体介导的胞饮作用。
Protein kinase C activators inhibit receptor-mediated potocytosis by preventing internalization of caveolae.
作者信息
Smart E J, Foster D C, Ying Y S, Kamen B A, Anderson R G
机构信息
Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, Dallas 75235.
出版信息
J Cell Biol. 1994 Feb;124(3):307-13. doi: 10.1083/jcb.124.3.307.
Abstract
Potocytosis is an endocytic pathway that utilizes glycosylphosphatidylinositol-anchored membrane proteins and caveolae to concentrate and internalize small molecules. We now report that activators of protein kinase C are potent inhibitors of potocytosis. Activators such as phorbol-12-myristate-13-acetate (PMA) inhibit the internalization of receptors for 5-methyltetrahydrofolate but allow the internal receptor pool to return to the cell surface. PMA does not affect the clustering of the folate receptor but instead markedly reduces the number of caveolae. Exposure to PMA totally blocks the intracellular accumulation of 5-methyltetrahydrofolate without affecting receptor-independent uptake or the formation of polyglutamylated species of 5-methyltetrahydrofolate in the cytoplasm. These data suggest that PMA inhibits uptake by inactivating caveolae internalization.
摘要
小窝蛋白介导的内吞作用是一种内吞途径，它利用糖基磷脂酰肌醇锚定膜蛋白和小窝来浓缩和内化小分子。我们现在报告蛋白激酶C的激活剂是小窝蛋白介导的内吞作用的有效抑制剂。诸如佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA）等激活剂抑制5-甲基四氢叶酸受体的内化，但允许内化的受体池返回细胞表面。PMA不影响叶酸受体的聚集，而是显著减少小窝的数量。暴露于PMA会完全阻断5-甲基四氢叶酸的细胞内积累，而不影响受体非依赖性摄取或细胞质中5-甲基四氢叶酸多聚谷氨酸化物种的形成。这些数据表明，PMA通过使小窝内化失活来抑制摄取。
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Protein kinase C activators inhibit receptor-mediated potocytosis by preventing internalization of caveolae.蛋白激酶C激活剂通过阻止小窝内吞作用来抑制受体介导的胞饮作用。
J Cell Biol. 1994 Feb;124(3):307-13. doi: 10.1083/jcb.124.3.307.
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