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本文引用的文献

1
The polarity protein Angiomotin p130 controls dendritic spine maturation.极性蛋白 Angiomotin p130 控制树突棘成熟。
J Cell Biol. 2018 Feb 5;217(2):715-730. doi: 10.1083/jcb.201705184. Epub 2018 Jan 9.
2
Cell Polarity in Yeast.酵母细胞极性。
Annu Rev Cell Dev Biol. 2017 Oct 6;33:77-101. doi: 10.1146/annurev-cellbio-100616-060856. Epub 2017 Aug 7.
3
Loss of Mpdz impairs ependymal cell integrity leading to perinatal-onset hydrocephalus in mice.Mpdz缺失会损害室管膜细胞的完整性,导致小鼠围产期脑积水。
EMBO Mol Med. 2017 Jul;9(7):890-905. doi: 10.15252/emmm.201606430.
4
Ran-dependent TPX2 activation promotes acentrosomal microtubule nucleation in neurons.Ran 依赖性的 TPX2 激活促进神经元中无中心体微管的核形成。
Sci Rep. 2017 Feb 13;7:42297. doi: 10.1038/srep42297.
5
Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.细胞特异性的丙酮酸激酶同工型有助于维持不同形式的持续性长期突触可塑性。
J Neurosci. 2017 Mar 8;37(10):2746-2763. doi: 10.1523/JNEUROSCI.2805-16.2017. Epub 2017 Feb 8.
6
DLG5 connects cell polarity and Hippo signaling protein networks by linking PAR-1 with MST1/2.DLG5通过将PAR-1与MST1/2连接起来,连接细胞极性和Hippo信号蛋白网络。
Genes Dev. 2016 Dec 15;30(24):2696-2709. doi: 10.1101/gad.284539.116.
7
Roles of afadin in the formation of the cellular architecture of the mouse hippocampus and dentate gyrus.afadin在小鼠海马体和齿状回细胞结构形成中的作用。
Mol Cell Neurosci. 2017 Mar;79:34-44. doi: 10.1016/j.mcn.2016.12.007. Epub 2016 Dec 29.
8
Planar cell polarity genes Frizzled3a, Vangl2, and Scribble are required for spinal commissural axon guidance.平面细胞极性基因卷曲蛋白3a、Vangl2和scribble是脊髓连合轴突导向所必需的。
BMC Neurosci. 2016 Dec 12;17(1):83. doi: 10.1186/s12868-016-0318-z.
9
Regulation of aPKC activity by Nup358 dependent SUMO modification.通过Nup358依赖性SUMO修饰对非典型蛋白激酶C(aPKC)活性的调控
Sci Rep. 2016 Sep 29;6:34100. doi: 10.1038/srep34100.
10
Dual function of partitioning-defective 3 in the regulation of YAP phosphorylation and activation.细胞分裂缺陷蛋白3在YAP磷酸化和激活调控中的双重功能
Cell Discov. 2016 Jul 5;2:16021. doi: 10.1038/celldisc.2016.21. eCollection 2016.

神经元极化中的 PAR3-PAR6-非典型 PKC 极性复合物蛋白。

PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.

机构信息

Department of Medicine, School of Medicine, University of Minnesota, 401 East River Parkway, Minneapolis, MN, 55455, USA.

Department of Immunobiology, School of Medicine, Yale University, 300 Cedar Street, New Haven, CT, 06520, USA.

出版信息

Cell Mol Life Sci. 2018 Aug;75(15):2735-2761. doi: 10.1007/s00018-018-2828-6. Epub 2018 Apr 25.

DOI:10.1007/s00018-018-2828-6
PMID:29696344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11105418/
Abstract

Polarity is a fundamental feature of cells. Protein complexes, including the PAR3-PAR6-aPKC complex, have conserved roles in establishing polarity across a number of eukaryotic cell types. In neurons, polarity is evident as distinct axonal versus dendritic domains. The PAR3, PAR6, and aPKC proteins also play important roles in neuronal polarization. During this process, either aPKC kinase activity, the assembly of the PAR3-PAR6-aPKC complex or the localization of these proteins is regulated downstream of a number of signaling pathways. In turn, the PAR3, PAR6, and aPKC proteins control various effector molecules to establish neuronal polarity. Herein, we discuss the many signaling mechanisms and effector functions that have been linked to PAR3, PAR6, and aPKC during the establishment of neuronal polarity.

摘要

极性是细胞的基本特征。包括 PAR3-PAR6-aPKC 复合物在内的蛋白质复合物在许多真核细胞类型中建立极性方面具有保守作用。在神经元中,极性表现为明显的轴突与树突域。PAR3、PAR6 和 aPKC 蛋白在神经元极化中也发挥着重要作用。在此过程中,aPKC 激酶活性、PAR3-PAR6-aPKC 复合物的组装或这些蛋白的定位受许多信号通路的下游调控。反过来,PAR3、PAR6 和 aPKC 蛋白控制各种效应分子来建立神经元极性。在此,我们讨论了在建立神经元极性过程中与 PAR3、PAR6 和 aPKC 相关的许多信号机制和效应功能。