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2022, 04, v.41 919-926
Pink1/Parkin信号通路调控线粒体自噬的研究进展
基金项目(Foundation): 国家自然科学基金项目(81973774)资助
邮箱(Email): ljh18817424778@163.com;
DOI: 10.13417/j.gab.041.000919
摘要:

线粒体自噬是指为了维持细胞内环境稳定而通过选择性自噬来降解功能失调或过剩的线粒体。在众多线粒体自噬相关通路研究中,对Pink1/Parkin信号通路的探索较为详细。在哺乳动物细胞中,Ser/Thr蛋白激酶Pink1和E3泛素连接酶Parkin协同作用,感知线粒体功能状态并对受损的线粒体进行标记,以促进其通过自噬途径进行降解。同时,泛素化和去泛素化在调节Parkin和线粒体自噬活性中起着重要的作用。本文就Pink1/Parkin信号通路以及去泛素化酶在线粒体自噬中的作用进行综述。

Abstract:

Mitochondrial autophagy refers to the selective autophagy to remove dysfunctional or excessive mitochondria in order to maintain the stability of intracellular homeostasis. The Pink1/Parkin signaling pathway is most widely studied in mitochondrial autophagy-related pathways. In mammalian cells, the Ser/Thr kinase Pink1 and the E3 ubiquitin ligase Parkin synergistically act to sense mitochondrial status and tag damaged mitochondria for autophagic degradation through autophagy pathways. Meanwhile, ubiquitination and deubiquitination enzymes play important roles in regulating Parkin activity and efficiency of mitochondrial autophagy. In this review, the Pink1/Parkin signaling pathway and the roles of deubiquitination enzymes in mitochondrial autophagy are discussed.

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基本信息:

DOI:10.13417/j.gab.041.000919

中图分类号:Q343

引用信息:

[1]王香香,凌江红,王煜姣,等.Pink1/Parkin信号通路调控线粒体自噬的研究进展[J].基因组学与应用生物学,2022,41(04):919-926.DOI:10.13417/j.gab.041.000919.

基金信息:

国家自然科学基金项目(81973774)资助

发布时间:

2022-04-25

出版时间:

2022-04-25

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