Negative regulation of fibroblast motility by Ena/VASP proteins
Negative regulation of fibroblast motility by Ena/VASP proteins
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DOI：
10.1016/s0092-8674(00)80884-3
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发表时间：
2000-06-23
期刊：
影响因子：
64.5
通讯作者：
Gertler, FB
中科院分区：
文献类型：
--
作者：
Bear, JE;Loureiro, JJ;Gertler, FB
Ena/VASP蛋白通过调节肌动蛋白细胞骨架参与细胞运动，并在粘着斑和前缘发现。使用过表达，功能丧失和抑制的方法，我们发现，Ena/VASP蛋白负调节成纤维细胞运动。当Ena/VASP蛋白在成纤维细胞中过表达时，观察到运动的密切依赖性降低。所有Ena/VASP蛋白的中和或缺失导致细胞运动增加。选择性去除局灶性粘连中的Ena/VASP蛋白，而不是前缘，对运动性没有影响。Ena/VASP蛋白的组成性膜靶向抑制运动性。这些结果是在显着的对比，目前的模型Ena/VASP功能主要来自他们的作用，肌动蛋白驱动的运动单核细胞增生李斯特菌。
Ena/VASP proteins have been implicated in cell motility through regulation of the actin cytoskeleton and are found at focal adhesions and the leading edge. Using overexpression, loss-of-function, and inhibitory approaches, we find that Ena/VASP proteins negatively regulate fibroblast motility. A close-dependent decrease in movement is observed when Ena/VASP proteins are overexpressed in fibroblasts. Neutralization or deletion of all Ena/VASP proteins results in increased cell movement. Selective depletion of Ena/VASP proteins from focal adhesions, but not the leading edge, has no effect on motility. Constitutive membrane targeting of Ena/VASP proteins inhibits motility. These results are in marked contrast to current models for Ena/VASP function derived mainly from their role in the actin-driven movement of Listeria monocytogenes.