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本文引用的文献

1
TRIM37, a novel E3 ligase for PEX5-mediated peroxisomal matrix protein import.TRIM37,一种用于PEX5介导的过氧化物酶体基质蛋白导入的新型E3连接酶。
J Cell Biol. 2017 Sep 4;216(9):2843-2858. doi: 10.1083/jcb.201611170. Epub 2017 Jul 19.
2
The peroxisomal AAA ATPase complex prevents pexophagy and development of peroxisome biogenesis disorders.过氧化物酶体AAA ATP酶复合体可防止过氧化物酶体自噬及过氧化物酶体生物发生障碍的发展。
Autophagy. 2017 May 4;13(5):868-884. doi: 10.1080/15548627.2017.1291470.
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Cleaning House: Selective Autophagy of Organelles.清理门户:细胞器的选择性自噬
Dev Cell. 2017 Apr 10;41(1):10-22. doi: 10.1016/j.devcel.2017.02.016.
4
Pexophagy is responsible for 65% of cases of peroxisome biogenesis disorders.过氧化物酶体自噬导致了65%的过氧化物酶体生物发生障碍病例。
Autophagy. 2017 May 4;13(5):991-994. doi: 10.1080/15548627.2017.1291480. Epub 2017 Feb 28.
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Assays to Monitor Pexophagy in Yeast.监测酵母中pexophagy的实验方法。
Methods Enzymol. 2017;588:413-427. doi: 10.1016/bs.mie.2016.09.088. Epub 2016 Nov 30.
6
Newly born peroxisomes are a hybrid of mitochondrial and ER-derived pre-peroxisomes.新生成的过氧化物酶体是线粒体和内质网衍生的前过氧化物酶体的杂交体。
Nature. 2017 Feb 9;542(7640):251-254. doi: 10.1038/nature21375. Epub 2017 Feb 1.
7
PEX2 is the E3 ubiquitin ligase required for pexophagy during starvation.PEX2是饥饿期间线粒体自噬所需的E3泛素连接酶。
J Cell Biol. 2016 Sep 12;214(6):677-90. doi: 10.1083/jcb.201511034. Epub 2016 Sep 5.
8
Mechanistic insights into selective autophagy pathways: lessons from yeast.对选择性自噬途径的机制性见解:来自酵母的经验教训。
Nat Rev Mol Cell Biol. 2016 Sep;17(9):537-52. doi: 10.1038/nrm.2016.74. Epub 2016 Jul 6.
9
Assembly, maintenance and dynamics of peroxisomes.过氧化物酶体的组装、维持及动态变化
Biochim Biophys Acta. 2016 May;1863(5):787-9. doi: 10.1016/j.bbamcr.2016.01.020. Epub 2016 Feb 3.
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Sharing with your children: Mechanisms of peroxisome inheritance.与您的孩子分享:过氧化物酶体遗传机制。
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PEX5 泛素化在维持过氧化物酶体动态平衡和稳态中的作用。

Role of PEX5 ubiquitination in maintaining peroxisome dynamics and homeostasis.

机构信息

a Section of Molecular Biology, Division of Biological Sciences , University of California, San Diego , La Jolla , CA , USA.

出版信息

Cell Cycle. 2017;16(21):2037-2045. doi: 10.1080/15384101.2017.1376149. Epub 2017 Sep 21.

DOI:10.1080/15384101.2017.1376149
PMID:28933989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5731411/
Abstract

Peroxisomes are essential and dynamic organelles that allow cells to rapidly adapt and cope with changing environments and/or physiological conditions by modulation of both peroxisome biogenesis and turnover. Peroxisome biogenesis involves the assembly of peroxisome membranes and the import of peroxisomal matrix proteins. The latter depends on the receptor, PEX5, which recognizes peroxisomal matrix proteins in the cytosol directly or indirectly, and transports them to the peroxisomal lumen. In this review, we discuss the role of PEX5 ubiquitination in both peroxisome biogenesis and turnover, specifically in PEX5 receptor recycling, stability and abundance, as well as its role in pexophagy (autophagic degradation of peroxisomes).

摘要

过氧化物酶体是必不可少的和动态的细胞器,通过调节过氧化物酶体的生物发生和周转率,使细胞能够快速适应和应对不断变化的环境和/或生理条件。过氧化物酶体的生物发生涉及过氧化物酶体膜的组装和过氧化物酶体基质蛋白的导入。后者依赖于受体 PEX5,它直接或间接地识别细胞质中的过氧化物酶体基质蛋白,并将它们运输到过氧化物酶体腔中。在这篇综述中,我们讨论了 PEX5 泛素化在过氧化物酶体生物发生和周转率中的作用,特别是在 PEX5 受体回收、稳定性和丰度,以及在过氧化物酶体自噬(过氧化物酶体的自噬降解)中的作用。