蛋白质稳态
热休克蛋白
热冲击
细胞生物学
生物
效应器
高铁F1
热冲击系数
热休克蛋白70
伴侣(临床)
细胞应激反应
战斗或逃跑反应
遗传学
医学
基因
病理
作者
Benjamin Lang,Martín Guerrero,Thomas Prince,Yuka Okusha,Cristina Bonorino,Stuart K. Calderwood
标识
DOI:10.1007/s00204-021-03070-8
摘要
Cells respond to protein-damaging (proteotoxic) stress by activation of the Heat Shock Response (HSR). The HSR provides cells with an enhanced ability to endure proteotoxic insults and plays a crucial role in determining subsequent cell death or survival. The HSR is, therefore, a critical factor that influences the toxicity of protein stress. While named for its vital role in the cellular response to heat stress, various components of the HSR system and the molecular chaperone network execute essential physiological functions as well as responses to other diverse toxic insults. The effector molecules of the HSR, the Heat Shock Factors (HSFs) and Heat Shock Proteins (HSPs), are also important regulatory targets in the progression of neurodegenerative diseases and cancers. Modulation of the HSR and/or its extended network have, therefore, become attractive treatment strategies for these diseases. Development of effective therapies will, however, require a detailed understanding of the HSR, important features of which continue to be uncovered and are yet to be completely understood. We review recently described and hallmark mechanistic principles of the HSR, the regulation and functions of HSPs, and contexts in which the HSR is activated and influences cell fate in response to various toxic conditions.
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