Cellular maintenance of nuclear protein homeostasis.
Cellular maintenance of nuclear protein homeostasis.
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DOI：
10.1007/s00018-013-1530-y
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发表时间：
2014-05
影响因子：
8
通讯作者：
Gardner, Richard G.
中科院分区：
文献类型：
--
作者：
Gallagher, Pamela S.;Oeser, Michelle L.;Abraham, Ayelet-chen;Kaganovich, Daniel;Gardner, Richard G.
关键词：
错误折叠的蛋白质的积累和聚集是45种以上人类退行性疾病的主要标志。这些破坏性的疾病包括阿尔茨海默氏症、帕金森氏症、亨廷顿氏症和肌萎缩侧索硬化症(ALS)。超过15种退行性疾病与错误折叠的蛋白质聚集有关，特别是在细胞核中。但是，细胞如何保护细胞核免受错误折叠的蛋白质的影响还不完全清楚。在这篇综述中，我们讨论了目前已知的维持细胞核内蛋白质稳态和保护细胞核免受错误折叠的蛋白质聚集和聚集的细胞机制。特别是，我们关注在应激过程中发现的定位于细胞核的伴侣蛋白，富含在细胞核中的泛素-蛋白酶体成分，可能存在于细胞核中协调折叠和降解的信号系统，以及与细胞核相关的错误折叠蛋白质沉积的位置。
The accumulation and aggregation of misfolded proteins is the primary hallmark for more than 45 human degenerative diseases. These devastating disorders include Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis (ALS). Over 15 degenerative diseases are associated with the aggregation of misfolded proteins specifically in the nucleus of cells. But, how the cell safeguards the nucleus from misfolded proteins is not entirely clear. In this review, we discuss what is currently known about the cellular mechanisms that maintain protein homeostasis in the nucleus and protect the nucleus from misfolded protein accumulation and aggregation. In particular, we focus on the chaperones found to localize to the nucleus during stress, the ubiquitin-proteasome components enriched in the nucleus, the signaling systems that might be present in the nucleus to coordinate folding and degradation, and the sites of misfolded protein deposition associated with the nucleus.
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