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本文引用的文献

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J Cell Biol. 2008 Mar 24;180(6):1177-89. doi: 10.1083/jcb.200709080.
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Synaptic protein degradation underlies destabilization of retrieved fear memory.突触蛋白降解是消退恐惧记忆不稳定的基础。
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The requirement for Phr1 in CNS axon tract formation reveals the corticostriatal boundary as a choice point for cortical axons.中枢神经系统轴突束形成过程中对Phr1的需求揭示了皮质纹状体边界是皮质轴突的一个选择点。
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泛素蛋白酶体系统在突触重塑和神经退行性疾病中的作用。

The role of the ubiquitin proteasome system in synapse remodeling and neurodegenerative diseases.

作者信息

Ding Mei, Shen Kang

机构信息

Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.

出版信息

Bioessays. 2008 Nov;30(11-12):1075-83. doi: 10.1002/bies.20843.

DOI:10.1002/bies.20843
PMID:18937340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3095215/
Abstract

The ubiquitin proteasome system is a potent regulatory mechanism used to control protein stability in numerous cellular processes, including neural development. Many neurodegenerative diseases are featured by the accumulation of UPS-associated proteins, suggesting the UPS dysfunction may be crucial for pathogenesis. Recent experiments have highlighted the UPS as a key player during synaptic development. Here we summarize recent discoveries centered on the role of the UPS in synapse remodeling and draw attention to the potential link between the synaptic UPS dysfunction and the pathology of neurodegenerative diseases.

摘要

泛素蛋白酶体系统是一种强大的调节机制,用于在包括神经发育在内的众多细胞过程中控制蛋白质稳定性。许多神经退行性疾病的特征是与泛素蛋白酶体系统相关的蛋白质积累,这表明泛素蛋白酶体系统功能障碍可能对发病机制至关重要。最近的实验突出了泛素蛋白酶体系统在突触发育过程中的关键作用。在这里,我们总结了围绕泛素蛋白酶体系统在突触重塑中的作用的最新发现,并提请注意突触泛素蛋白酶体系统功能障碍与神经退行性疾病病理学之间的潜在联系。