Gelsolin overexpression enhances neurite outgrowth in PC12 cells
Gelsolin overexpression enhances neurite outgrowth in PC12 cells
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DOI：
10.1016/s0014-5793(01)03078-2
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发表时间：
2001-11-16
期刊：
影响因子：
3.5
通讯作者：
Schmidt, CE
中科院分区：
文献类型：
--
作者：
Furnish, EJ;Zhou, W;Schmidt, CE
合理设计治疗神经损伤的疗法需要了解神经突延伸的机制。神经突运动由肌动蛋白聚合驱动；然而，其机制尚不清楚。一种肌动蛋白附属蛋白凝胶蛋白参与细胞骨架的重塑，尽管其在细胞运动中的作用尚不清楚。我们报告两倍上调凝胶与神经生长因子分化。与对照组相比，基因修饰过表达凝胶蛋白的细胞具有更长的神经突和更大的神经突运动率。这些数据表明凝胶在神经突生长中起重要作用。(C) 2001年由Elsevier Science B.V.代表欧洲生化学会联合会出版。
The rational design of therapies for treating nerve injuries requires an understanding of the mechanisms underlying neurite extension. Neurite motility is driven by actin polymerization; however, the mechanisms are not clearly understood. One actin accessory protein, gelsolin, is involved with remodeling the cytoskeleton, although its role in cell motility is unclear. We report a two-fold upregulation of gelsolin upon differentiation with nerve growth factor. Cells that were genetically modified to overexpress gelsolin have longer neurites and a greater neurite motility rate compared to controls. These data suggest that gelsolin plays an important role in neurite outgrowth. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.