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首页> 外文期刊>Cellular Signalling >Non-prenylatable, cytosolic Rac1 alters neurite outgrowth while retaining the ability to be activated
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Non-prenylatable, cytosolic Rac1 alters neurite outgrowth while retaining the ability to be activated

机译：不可胎早生的胞质Rac1改变神经突的生长，同时保留被激活的能力

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摘要

Rac1 is an important regulator of axon extension, cell migration and actin reorganization. Like all Rho guanine triphosphatases (GTPases), Rac1 is targeted to the membrane by the addition of a geranylgeranyl moiety, an action thought to result in Rac1 guanosine triphosphate (GTP) binding. However, the role that Rac1 localization plays in its activation (GTP loading) and subsequent activation of effectors is not completely clear. To address this, we developed a non-prenylatable emerald green fluorescent protein (EmGFP)-Rac1 fusion protein (EmGFP-Rac1(C189A)) and assessed how expressing this construct affected neurite outgrowth, Rac1 localization and activation in neuroblastoma cells. Expression of EmGFP-Rac1(C189A) increased localization to the cytosol and induced cell clustering while increasing neurite initiation. EmGFP-Rac1(C189A) expression also increased Rac1 activation in the cytosol, compared to cells expressing wild-type Rac1 (EmGFP-Rac1). These results suggest that activation of Rac1 may not require plasma membrane localization, potentially leading to differential activation of cytosolic signaling pathways that alter cell morphology. Understanding the consequences of differential localization and activation of Rho GTPases, including Rac1, could lead to new therapeutic targets for treating neurological disorders. (C) 2014 Elsevier Inc. All rights reserved.
机译：Rac1是轴突延伸，细胞迁移和肌动蛋白重组的重要调节器。像所有Rho鸟嘌呤三磷酸酶（GTPases）一样，Rac1通过添加香叶基香叶基（geranylgeranyl）部分而靶向膜，该作用被认为导致Rac1鸟苷三磷酸（GTP）结合。但是，Rac1定位在其激活（GTP加载）和效应子的后续激活中所起的作用尚不完全清楚。为了解决这个问题，我们开发了一种不可异戊二烯的翠绿色荧光蛋白（EmGFP）-Rac1融合蛋白（EmGFP-Rac1（C189A）），并评估了该构建体的表达如何影响神经突瘤细胞的生长，Rac1的定位和活化。 EmGFP-Rac1（C189A）的表达增加了对细胞质的定位并诱导了细胞的聚集，同时增加了神经突的起始。与表达野生型Rac1（EmGFP-Rac1）的细胞相比，EmGFP-Rac1（C189A）表达还增加了细胞溶胶中Rac1的活化。这些结果表明，Rac1的激活可能不需要质膜定位，从而可能导致改变细胞形态的胞质信号通路的差异激活。了解包括Rac1在内的Rho GTPases的差异化定位和激活的后果，可能会导致治疗神经系统疾病的新治疗靶点。 （C）2014 Elsevier Inc.保留所有权利。

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