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分支肌动蛋白网络在障碍物上的生长。

Growth of branched actin networks against obstacles.

作者信息

Carlsson A E

机构信息

Department of Physics, Washington University, St. Louis, Missouri 63130-4899, USA.

出版信息

Biophys J. 2001 Oct;81(4):1907-23. doi: 10.1016/S0006-3495(01)75842-0.

DOI:10.1016/S0006-3495(01)75842-0
PMID:11566765
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1301666/
Abstract

A method for simulating the growth of branched actin networks against obstacles has been developed. The method is based on simple stochastic events, including addition or removal of monomers at filament ends, capping of filament ends, nucleation of branches from existing filaments, and detachment of branches; the network structure for several different models of the branching process has also been studied. The models differ with regard to their inclusion of effects such as preferred branch orientations, filament uncapping at the obstacle, and preferential branching at filament ends. The actin ultrastructure near the membrane in lamellipodia is reasonably well produced if preferential branching in the direction of the obstacle or barbed-end uncapping effects are included. Uncapping effects cause the structures to have a few very long filaments that are similar to those seen in pathogen-induced "actin tails." The dependence of the growth velocity, branch spacing, and network density on the rate parameters for the various processes is quite different among the branching models. An analytic theory of the growth velocity and branch spacing of the network is described. Experiments are suggested that could distinguish among some of the branching models.

摘要

一种模拟分支肌动蛋白网络在障碍物上生长的方法已经被开发出来。该方法基于简单的随机事件,包括在细丝末端添加或去除单体、细丝末端的封端、从现有细丝上形成分支的成核以及分支的脱离;还研究了几种不同分支过程模型的网络结构。这些模型在是否包含诸如优先分支方向、障碍物处细丝的解封以及细丝末端的优先分支等效应方面存在差异。如果包含在障碍物方向上的优先分支或带刺末端解封效应,那么片状伪足中靠近膜的肌动蛋白超微结构就能得到较好的呈现。解封效应会使结构具有一些非常长的细丝,类似于在病原体诱导的“肌动蛋白尾巴”中看到的那些细丝。在不同的分支模型中,生长速度、分支间距和网络密度对各种过程速率参数的依赖性有很大差异。描述了网络生长速度和分支间距的解析理论。提出了一些能够区分某些分支模型的实验。

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本文引用的文献

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Activation by Cdc42 and PIP(2) of Wiskott-Aldrich syndrome protein (WASp) stimulates actin nucleation by Arp2/3 complex.威斯科特-奥尔德里奇综合征蛋白(WASp)被Cdc42和磷脂酰肌醇-4,5-二磷酸(PIP(2))激活后,会刺激肌动蛋白相关蛋白2/3复合体(Arp2/3 complex)介导的肌动蛋白成核作用。
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The Arp2/3 complex branches filament barbed ends: functional antagonism with capping proteins.肌动蛋白相关蛋白2/3复合体使丝状肌动蛋白的带刺末端分支:与封端蛋白的功能拮抗作用。
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