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信号调节的肌动蛋白解聚因子/丝切蛋白活性与生长锥运动性。

Signal-regulated ADF/cofilin activity and growth cone motility.

作者信息

Meberg P J

机构信息

Department of Biology, University of North Dakota, Grand Forks 58202, USA.

出版信息

Mol Neurobiol. 2000 Feb-Apr;21(1-2):97-107. doi: 10.1385/MN:21:1-2:097.

DOI:10.1385/MN:21:1-2:097
PMID:11327152
Abstract

It is becoming increasingly evident that proteins of the actin depolymerizing factor (ADF)/cofilin family are essential regulators of actin turnover required for many actin-based cellular processes, including motility. ADF can increase actin turnover by either increasing the rate of actin filament treadmilling or by severing actin filaments. In neurons ADF is highly expressed in neuronal growth cones and its activity is regulated by many signals that affect growth cone motility. In addition, increased activity of ADF causes an increase in neurite extension. ADF activity is inhibited upon phosphorylation by LIM kinases (LIMK), kinases activated by members of the Rho family of small GTPases. ADF become dephosphorylated downstream of signal pathways that activate PI-3 kinase or increase levels of intracellular calcium. The growth-regulating effects of ADF together with its ability to be regulated by a wide variety of guidance cues, suggest that ADF may regulate growth cone advance and navigation.

摘要

越来越明显的是,肌动蛋白解聚因子(ADF)/丝切蛋白家族的蛋白质是许多基于肌动蛋白的细胞过程(包括运动)所需的肌动蛋白周转的重要调节因子。ADF可以通过增加肌动蛋白丝踏车运动的速率或切断肌动蛋白丝来增加肌动蛋白周转。在神经元中,ADF在神经元生长锥中高度表达,其活性受许多影响生长锥运动的信号调节。此外,ADF活性增加会导致神经突延伸增加。ADF活性在被LIM激酶(LIMK)磷酸化后受到抑制,LIM激酶是由小GTP酶的Rho家族成员激活的激酶。ADF在激活PI-3激酶或增加细胞内钙水平的信号通路下游去磷酸化。ADF的生长调节作用及其受多种导向线索调节的能力表明,ADF可能调节生长锥的前进和导航。

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