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Cell Metab. 2019 Apr 2;29(4):979-992.e4. doi: 10.1016/j.cmet.2018.11.007. Epub 2018 Dec 6.
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Miro proteins prime mitochondria for Parkin translocation and mitophagy.Miro 蛋白使线粒体为 Parkin 易位和线粒体自噬做好准备。
EMBO J. 2019 Jan 15;38(2). doi: 10.15252/embj.201899384. Epub 2018 Nov 30.
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Biochem Biophys Res Commun. 2018 Dec 9;507(1-4):319-323. doi: 10.1016/j.bbrc.2018.11.031. Epub 2018 Nov 16.
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Mitochondrial dynamics, a key executioner in neurodegenerative diseases.线粒体动力学,神经退行性疾病的关键执行者。
Mitochondrion. 2019 Jul;47:151-173. doi: 10.1016/j.mito.2018.11.002. Epub 2018 Nov 5.
6
Loss of the mitochondrial -AAA protease YME1L leads to ocular dysfunction and spinal axonopathy.线粒体 -AAA 蛋白酶 YME1L 的缺失导致眼部功能障碍和脊髓轴突变性。
EMBO Mol Med. 2019 Jan;11(1). doi: 10.15252/emmm.201809288.
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Deciphering OPA1 mutations pathogenicity by combined analysis of human, mouse and yeast cell models.通过对人、鼠和酵母细胞模型的综合分析来破译 OPA1 突变的致病性。
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8
Regulation of ER-mitochondria contacts by Parkin via Mfn2.Parkin 通过 Mfn2 调节 ER-线粒体接触。
Pharmacol Res. 2018 Dec;138:43-56. doi: 10.1016/j.phrs.2018.09.006. Epub 2018 Sep 13.
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Ablation of the stress protease OMA1 protects against heart failure in mice.应激蛋白酶 OMA1 的消融可预防小鼠心力衰竭。
Sci Transl Med. 2018 Mar 28;10(434). doi: 10.1126/scitranslmed.aan4935.
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m-AAA and i-AAA complexes coordinate to regulate OMA1, the stress-activated supervisor of mitochondrial dynamics.m-AAA 和 i-AAA 复合物协调调节 OMA1,即应激激活的线粒体动力学监督因子。
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线粒体动力学的蛋白水解调节。

Proteolytic regulation of mitochondrial dynamics.

机构信息

Department of Biochemistry, University of Nebraska, Lincoln, NE 68588, United States of America.

Department of Biochemistry, University of Nebraska, Lincoln, NE 68588, United States of America; Nebraska Redox Biology Center, University of Nebraska, Lincoln, NE 68588, United States of America; Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States of America.

出版信息

Mitochondrion. 2019 Nov;49:289-304. doi: 10.1016/j.mito.2019.04.008. Epub 2019 Apr 25.

DOI:10.1016/j.mito.2019.04.008
PMID:31029640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6814530/
Abstract

Spatiotemporal changes in the abundance, shape, and cellular localization of the mitochondrial network, also known as mitochondrial dynamics, are now widely recognized to play a key role in mitochondrial and cellular physiology as well as disease states. This process involves coordinated remodeling of the outer and inner mitochondrial membranes by conserved dynamin-like guanosine triphosphatases and their partner molecules in response to various physiological and stress stimuli. Although the core machineries that mediate fusion and partitioning of the mitochondrial network have been extensively characterized, many aspects of their function and regulation are incompletely understood and only beginning to emerge. In the present review we briefly summarize current knowledge about how the key mitochondrial dynamics-mediating factors are regulated via selective proteolysis by mitochondrial and cellular proteolytic machineries.

摘要

线粒体网络的丰度、形态和细胞定位的时空变化,也称为线粒体动力学,现在被广泛认为在线粒体和细胞生理学以及疾病状态中发挥关键作用。这个过程涉及到保守的类似于 dynamin 的鸟苷三磷酸酶及其伴侣分子通过对外膜和内膜的协调重塑,以响应各种生理和应激刺激。尽管介导线粒体网络融合和分裂的核心机械已经得到广泛的描述,但它们的许多功能和调节方面仍不完全清楚,目前才刚刚开始出现。在本综述中,我们简要总结了目前关于关键线粒体动力学调节因子如何通过线粒体和细胞蛋白水解机制的选择性蛋白水解来调节的知识。