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肌动蛋白聚合导致膜弯曲。

Membrane bending by actin polymerization.

机构信息

Department of Physics, Washington University, One Brookings Drive, Campus Box 1105, St. Louis, MO 63130, United States.

出版信息

Curr Opin Cell Biol. 2018 Feb;50:1-7. doi: 10.1016/j.ceb.2017.11.007. Epub 2017 Dec 5.

DOI:10.1016/j.ceb.2017.11.007
PMID:29207306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5911415/
Abstract

Actin polymerization provides driving force to aid several types of processes that involve pulling the plasma membrane into the cell, including phagocytosis, cellular entry of large viruses, and endocytosis. In endocytosis, actin polymerization is especially important under conditions of high membrane tension or high turgor pressure. Recent modeling efforts have shown how actin polymerization can give rise to a distribution of forces around the endocytic site, and explored how these forces affect the shape dynamics; experiments have revealed the structure of the endocytic machinery in increasing detail, and demonstrated key feedback interactions between actin assembly and membrane curvature. Here we provide a perspective on these findings and suggest avenues for future research.

摘要

肌动蛋白聚合提供驱动力,有助于几种类型的过程,包括吞噬作用、大病毒进入细胞和胞吞作用,将质膜拉入细胞内。在胞吞作用中,当膜张力或膨压差较高时,肌动蛋白聚合尤为重要。最近的建模工作表明,肌动蛋白聚合如何在胞吞作用部位周围产生力的分布,并探讨了这些力如何影响形状动力学;实验越来越详细地揭示了胞吞作用机制的结构,并证明了肌动蛋白组装和膜曲率之间的关键反馈相互作用。在这里,我们提供了对这些发现的看法,并提出了未来研究的途径。

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本文引用的文献

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Actin growth profile in clathrin-mediated endocytosis.网格蛋白介导的胞吞作用中的肌动蛋白生长形态。
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