Targeted disruption of the gene for the PAK5 kinase in mice

Targeted disruption of the gene for the PAK5 kinase in mice
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DOI:
10.1128/mcb.23.20.7134-7142.2003
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发表时间:
2003-10-01
影响因子:
5.3
通讯作者:
Minden, A
Minden, A
中科院分区:
生物学2区
文献类型:
--
作者:
Li, XF;Minden, A

文献摘要

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PAK5是B组PAK丝氨酸/苏氨酸激酶家族的成员,也是Rho GTP酶CDc42的效应器。PAK5在大脑中高度表达,在其他几个组织中表达水平较低。在细胞系中,PAK5已被证明在丝状足的形成和轴突的生长中发挥作用。为了研究PAK5的生物学功能,我们在小鼠中缺失了PAK5基因。PAK5缺失的小鼠的表型与PAK4缺失的小鼠完全不同,PAK4是B组PAK家族的另一个成员。与胚胎致死的PAK4基因缺失的小鼠不同,PAK5基因缺失的小鼠发育正常,并具有生育能力。在没有PAK5的情况下,神经系统看起来是正常的,就像正常表达PAK5的其他组织一样。我们的结果表明,PAK5和其他Rho GTP酶靶标之间存在功能冗余。
PAK5 is a member of the group B family of PAK serine/threonine kinases and is an effector for the Rho GTPase Cdc42. PAK5 is highly expressed in the brain and is expressed at lower levels in several other tissues. In cell lines, PAK5 has been shown to play a role in filopodia formation and neurite outgrowth. To examine the biological function of PAK5, we deleted the PAK5 gene in mice. The phenotypes of the PAK5-null mice are completely different from those of mice null for PAK4, another member of the group B PAK family. Unlike PAK4-null mice, which are embryonic lethal, PAK5-null mice develop normally and are fertile. The nervous system appears normal in the absence of PAK5, as do other tissues in which PAK5 is normally expressed. Our results suggest functional redundancy between PAK5 and other Rho GTPase targets.