[关于 TANK 结合激酶 1 在 PINK1/Parkin 依赖性和非依赖性有丝分裂中的作用的研究进展]。

Q3 Medicine
生理学报 Pub Date : 2024-02-25
Hao Deng, Zhi Xia, Hua-Yu Shang
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引用次数: 0

摘要

线粒体吞噬是一个选择性清除多余或受损线粒体的过程,在调节细胞内线粒体质量和维持线粒体能量代谢方面发挥着重要作用。TANK 结合激酶 1(TBK1)是一种多功能丝氨酸/苏氨酸蛋白激酶,参与调控 PTEN 诱导的假定激酶 1(PINK1)/Parkin 依赖性和非依赖性有丝分裂。最近的研究表明,TBK1 可使自噬相关蛋白磷酸化,如光神经蛋白(OPTN)、p62/sequestosome-1、Ras 相关 GTP 结合蛋白 7(Rab7)、并介导核点蛋白 52(NDP52)与 UNC-51 类似自噬激活激酶 1(ULK1)复合物的结合,以及 TAX1 结合蛋白 1(TAX1BP1)与微管相关蛋白 1 轻链 3(LC3)的结合,从而增强 PINK1/Parkin 依赖性的有丝分裂。此外,TBK1还是AMP激活蛋白激酶(AMPK)/ULK1通路的直接底物,它的激活可使dynamin相关蛋白1(Drp1)和Rab7磷酸化,从而促进PINK1/Parkin依赖性有丝分裂。本文综述了 TBK1 在调控 PINK1/Parkin 依赖性和非依赖性有丝分裂中的作用和机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Research progress on the role of TANK-binding kinase 1 in PINK1/Parkin-dependent and -independent mitophagy].

Mitophagy is a process that selectively removes excess or damaged mitochondria and plays an important role in regulating intracellular mitochondrial mass and maintaining mitochondrial energy metabolism. TANK-binding kinase 1 (TBK1) is a multifunctional serine/threonine protein kinase, which is involved in the regulation of PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent and -independent mitophagy. Recent studies have shown that TBK1 phosphorylates the autophagy related proteins, such as optineurin (OPTN), p62/sequestosome-1, Ras-related GTP binding protein 7 (Rab7), and mediates the binding of nuclear dot protein 52 (NDP52) to UNC-51 like autophagy activating kinase 1 (ULK1) complex, as well as the binding of TAX1-binding protein 1 (TAX1BP1) to microtubule-associated protein 1 light chain 3 (LC3), thereby enhancing PINK1/Parkin-dependent mitophagy. In addition, TBK1 is a direct substrate of AMP-activated protein kinase (AMPK)/ULK1 pathway, and its activation phosphorylates dynamin-related protein 1 (Drp1) and Rab7 to promote PINK1/Parkin-independent mitophagy. This article reviews the role and mechanism of TBK1 in regulating PINK1/Parkin-dependent and -independent mitophagy.

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来源期刊
生理学报
生理学报 Medicine-Medicine (all)
CiteScore
1.20
自引率
0.00%
发文量
4820
期刊介绍: Acta Physiologica Sinica (APS) is sponsored by the Chinese Association for Physiological Sciences and Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences (CAS), and is published bimonthly by the Science Press, China. APS publishes original research articles in the field of physiology as well as research contributions from other biomedical disciplines and proceedings of conferences and symposia of physiological sciences. Besides “Original Research Articles”, the journal also provides columns as “Brief Review”, “Rapid Communication”, “Experimental Technique”, and “Letter to the Editor”. Articles are published in either Chinese or English according to authors’ submission.
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