Keski-Oja J, Alitalo K
Exp Cell Res. 1985 May;158(1):86-94. doi: 10.1016/0014-4827(85)90433-1.
Epithelial PtK2 cells were used as a model to study the possible redistribution of the major tyrosine protein kinase substrate, p36, upon drug-induced reorganization of the cytokeratin network. Cells were grown on glass coverslips and exposed to cytochalasin D (CD), colcemid or a combination of the two. The cytokeratin type intermediate filaments of the cells were redistributed by treatment of the cells with colchicine and CD. Simultaneous changes in cytokeratin and in p36 antigen were observed by double-label immunofluorescence. In control PtK2 cells, p36 was distributed characteristically at the cortical cytoplasm. Neither colchicine nor CD alone was able to cause a major reorganization of cytokeratin or p36. Their combined effect resulted in formation of blebs containing abundant p36 at the cell surface and at cell-cell junctions. Actin, on the other hand, was reorganized to similar configurations by CD alone. These observations show for the first time a drug-induced redistribution of p36. The results suggest a relationship between membrane-associated p36 and the cytoskeletal fibres that terminate at the plasma membrane.
上皮PtK2细胞被用作模型，以研究在药物诱导细胞角蛋白网络重组时，主要酪氨酸蛋白激酶底物p36可能的重新分布情况。细胞在玻璃盖玻片上生长，并暴露于细胞松弛素D（CD）、秋水仙酰胺或两者的组合中。用秋水仙碱和CD处理细胞后，细胞中的细胞角蛋白中间丝发生了重新分布。通过双标记免疫荧光观察到细胞角蛋白和p36抗原的同时变化。在对照PtK2细胞中，p36典型地分布在皮质细胞质中。单独使用秋水仙碱或CD都不能引起细胞角蛋白或p36的重大重组。它们的联合作用导致在细胞表面和细胞间连接处形成含有丰富p36的泡状突起。另一方面，肌动蛋白仅通过CD就被重组为类似的构型。这些观察首次表明了药物诱导的p36重新分布。结果表明膜相关p36与终止于质膜的细胞骨架纤维之间存在关联。
