核蛋白酶体作为自噬的后备力量:相互关联的蛋白稳态途径。

Meiyan Jin, Daniel J Klionsky
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引用次数: 0

摘要

蛋白质稳态(proteostasis)是指细胞蛋白质环境的平衡,它受到蛋白质合成、折叠、运输和降解途径的严格调控。越来越多的证据表明,这些途径相互关联,确保了蛋白质平衡网络的稳健性。Park 等人最近的一项研究表明,在大自噬/自噬缺陷细胞中,蛋白酶体或核孔成分的缺失会导致合成致死,因为在自噬受损情况下积累的细胞质蛋白质会被转运到细胞核并被核蛋白酶体降解。作者说明了亨廷顿病等情况下的细胞为什么更容易受到蛋白稳态干扰的机理基础:缩写:UPR:未折叠蛋白反应;UPS:泛素-蛋白酶体系统。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nuclear proteasomes as a backup for autophagy: interconnected proteostasis pathways.

Protein homeostasis (proteostasis) refers to the balance of the cellular protein environment, tightly regulated by pathways governing protein synthesis, folding, trafficking, and degradation. Growing evidence supports the interconnection of these pathways to ensure the robustness of the proteo-stasis network. A recent study by Park et al. showed that, in macroautophagy/autophagy-deficient cells, the loss of proteasome or nuclear pore components causes synthetic lethality, as cytoplasmic proteins that accumulate under impaired autophagy are transported to the nucleus and degraded by nuclear proteasomes. The authors illustrated the mechanistic basis for why cells with conditions such as Huntington disease, where both autophagy and cytoplasm-to-nuclear shuttling are compromised, are more vulnerable to proteostasis perturbation.Abbreviation: UPR: unfolded protein response; UPS: ubiquitin-proteasome system.

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