自噬
肌萎缩侧索硬化
应力颗粒
失智症
细胞生物学
疾病
蛋白质聚集
神经科学
额颞叶变性
神经退行性变
生物
医学
痴呆
遗传学
病理
细胞凋亡
基因
翻译(生物学)
信使核糖核酸
作者
Laura Ryan,David C. Rubinsztein
出处
期刊:FEBS Letters
[Wiley]
日期:2023-12-21
卷期号:598 (1): 59-72
被引量:5
标识
DOI:10.1002/1873-3468.14787
摘要
Our understanding of stress granule (SG) biology has deepened considerably in recent years, and with this, increased understanding of links has been made between SGs and numerous neurodegenerative diseases. One of the proposed mechanisms by which SGs and any associated protein aggregates may become pathological is based upon defects in their autophagic clearance, and so the precise processes governing the degradation of SGs are important to understand. Mutations and disease‐associated variants implicated in amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease and frontotemporal lobar dementia compromise autophagy, whilst autophagy‐inhibiting drugs or knockdown of essential autophagy proteins result in the persistence of SGs. In this review, we will consider the current knowledge regarding the autophagy of SG.
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