粒体自噬
线粒体
细胞生物学
生物
蛋白质稳态
DNAJA3公司
蛋白质组
线粒体融合
氧化磷酸化
线粒体DNA
自噬
生物化学
基因
细胞凋亡
作者
Laurie Lee-Glover,Timothy E. Shutt
标识
DOI:10.1016/j.tem.2023.11.004
摘要
Mitochondrial quality control (MQC) mechanisms are required to maintain a functional proteome, which enables mitochondria to perform a myriad of important cellular functions from oxidative phosphorylation to numerous other metabolic pathways. Mitochondrial protein homeostasis begins with the import of over 1000 nuclear-encoded mitochondrial proteins and the synthesis of 13 mitochondrial DNA-encoded proteins. A network of chaperones and proteases helps to fold new proteins and degrade unnecessary, damaged, or misfolded proteins, whereas more extensive damage can be removed by mitochondrial-derived vesicles (MDVs) or mitochondrial autophagy (mitophagy). Here, focusing on mechanisms in mammalian cells, we review the importance of mitochondrial protein import as a sentinel of mitochondrial function that activates multiple MQC mechanisms when impaired.
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