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Pak1作为Rac1在皮层神经元中的下游效应因子参与树突起始过程。

Pak1 is involved in dendrite initiation as a downstream effector of Rac1 in cortical neurons.

作者信息

Hayashi Kanehiro, Ohshima Toshio, Mikoshiba Katsuhiko

机构信息

Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN, Wako-shi, Saitama 351-0198, Japan.

出版信息

Mol Cell Neurosci. 2002 Aug;20(4):579-94. doi: 10.1006/mcne.2002.1144.

Abstract

Dendrite development in neurons is one of the bases for the formation of a complex neuronal network in the nervous system, and involvement of the Rho family GTPases, including Rac1, Cdc42, and RhoA, in dendrite formation has been demonstrated. One of the effectors of Rac1 and Cdc42, p21-activated kinase 1 (Pak1), is abundant in the brain; however, the function of Pak1 in neurons remains unknown. In order to clarify the roles of Pak1 in neurons, we introduced mutant Pak1 into immature neurons by a novel gene transfer technique using in utero electroporation. Introduction of constitutive active (CA)-Pak1 led to increase the number of dendrites, whereas introduction of dominant negative (DN)-Pak1 caused a reduction, and coexpression of CA-Rac1 and DN-Pak1 also resulted in a reduction in the number of dendrites. These results suggest that Pak1 regulates dendrite initiation as a downstream effector of Rac1.

摘要

神经元中的树突发育是神经系统中复杂神经网络形成的基础之一,并且已经证明包括Rac1、Cdc42和RhoA在内的Rho家族小G蛋白参与树突形成。Rac1和Cdc42的效应器之一,p21激活激酶1(Pak1),在大脑中含量丰富;然而,Pak1在神经元中的功能仍然未知。为了阐明Pak1在神经元中的作用,我们通过一种使用子宫内电穿孔的新型基因转移技术,将突变型Pak1导入未成熟神经元。组成型活性(CA)-Pak1的导入导致树突数量增加,而显性负性(DN)-Pak1的导入则导致树突数量减少,并且CA-Rac1和DN-Pak1的共表达也导致树突数量减少。这些结果表明,Pak1作为Rac1的下游效应器调节树突起始。

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