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神经疾病中的小泛素样修饰蛋白化作用

SUMOylation in Neurological Diseases.

作者信息

Liu F-Y, Liu Y-F, Yang Y, Luo Z-W, Xiang J-W, Chen Z-G, Qi R-L, Yang T-H, Xiao Y, Qing W-J, Li D W-C

机构信息

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong 510060,. China.

出版信息

Curr Mol Med. 2017;16(10):893-899. doi: 10.2174/1566524017666170109125256.

DOI:10.2174/1566524017666170109125256
PMID:28067168
Abstract

Since the discovery of SUMOs (small ubiquitin-like modifiers) over 20 years ago, sumoylation has recently emerged as an important posttranslational modification involved in almost all aspects of cellular physiology. In neurons, sumoylation dynamically modulates protein function and consequently plays an important role in neuronal maturation, synapse formation and plasticity. Thus, the dysfunction of sumoylation pathway is associated with many different neurological disorders. Hundreds of different proteins implicated in the pathogenesis of neurological disorders are SUMO-modified, indicating the importance of sumoylation involved in the neurological diseases. In this review, we summarize the growing findings on protein sumoylation in neuronal function and dysfunction. It is essential to have a thorough understanding on the mechanism how sumoylation contributes to neurological diseases in developing efficient therapy for these diseases.

摘要

自20多年前发现小泛素样修饰物(SUMOs)以来,SUMO化最近已成为一种重要的翻译后修饰,几乎涉及细胞生理学的各个方面。在神经元中,SUMO化动态调节蛋白质功能,因此在神经元成熟、突触形成和可塑性中发挥重要作用。因此,SUMO化途径的功能障碍与许多不同的神经疾病有关。数百种与神经疾病发病机制相关的不同蛋白质被SUMO修饰,这表明SUMO化在神经疾病中的重要性。在本综述中,我们总结了关于蛋白质SUMO化在神经元功能和功能障碍方面不断增加的研究结果。在开发针对这些疾病的有效治疗方法时,全面了解SUMO化如何导致神经疾病的机制至关重要。

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1
SUMOylation in Neurological Diseases.神经疾病中的小泛素样修饰蛋白化作用
Curr Mol Med. 2017;16(10):893-899. doi: 10.2174/1566524017666170109125256.
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Paromomycin targets HDAC1-mediated SUMOylation and IGF1R translocation in glioblastoma.巴龙霉素靶向胶质母细胞瘤中HDAC1介导的SUMO化和IGF1R易位。
Front Pharmacol. 2024 Dec 11;15:1490878. doi: 10.3389/fphar.2024.1490878. eCollection 2024.
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Knocking Down PIAS3 Reduces HO-induced Oxidative Stress Injury in HT22 Cells.敲低 PIAS3 减少 HT22 细胞中 HO 诱导的氧化应激损伤。
Cell Biochem Biophys. 2024 Jun;82(2):1381-1387. doi: 10.1007/s12013-024-01292-y. Epub 2024 May 11.
3
Proteomic Identification of an Endogenous Synaptic SUMOylome in the Developing Rat Brain.
发育中大鼠大脑内源性突触SUMO化蛋白质组的蛋白质组学鉴定
Front Mol Neurosci. 2021 Nov 23;14:780535. doi: 10.3389/fnmol.2021.780535. eCollection 2021.
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Variation in expression of small ubiquitin-like modifiers in injured sciatic nerve of mice.小鼠坐骨神经损伤后小泛素样修饰物表达的变化
Neural Regen Res. 2019 Aug;14(8):1455-1461. doi: 10.4103/1673-5374.253531.
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SUMO2/3 modification of activating transcription factor 5 (ATF5) controls its dynamic translocation at the centrosome.SUMO2/3 修饰激活转录因子 5(ATF5)控制其在中心体的动态易位。
J Biol Chem. 2018 Feb 23;293(8):2939-2948. doi: 10.1074/jbc.RA117.001151. Epub 2018 Jan 11.
6
SUMO, a small, but powerful, regulator of double-strand break repair.SUMO,一种双链断裂修复的小型但强大的调节因子。
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). doi: 10.1098/rstb.2016.0281.
7
Analysis of SUMO1-conjugation at synapses.突触处SUMO1缀合的分析。
Elife. 2017 Jun 9;6:e26338. doi: 10.7554/eLife.26338.