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细胞自噬:一场宿主与微生物之间的战斗

A Structural View of Xenophagy, a Battle between Host and Microbes.

机构信息

Department of Life Sciences, Korea University, Seoul 02841, Korea.

出版信息

Mol Cells. 2018 Jan 31;41(1):27-34. doi: 10.14348/molcells.2018.2274. Epub 2018 Jan 23.

DOI:10.14348/molcells.2018.2274
PMID:29370690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5792709/
Abstract

The cytoplasm in mammalian cells is a battlefield between the host and invading microbes. Both the living organisms have evolved unique strategies for their survival. The host utilizes a specialized autophagy system, xenophagy, for the clearance of invading pathogens, whereas bacteria secrete proteins to defend and escape from the host xenophagy. Several molecules have been identified and their structural investigation has enabled the comprehension of these mechanisms at the molecular level. In this review, we focus on one example of host autophagy and the other of bacterial defense: the autophagy receptor, NDP52, in conjunction with the sugar receptor, galectin-8, plays a critical role in targeting the autophagy machinery against ; and the cysteine protease, RavZ secreted by cleaves the LC3-PE on the phagophore membrane. The structure-function relationships of these two examples and the directions of future research will be discussed.

摘要

哺乳动物细胞的细胞质是宿主和入侵微生物之间的战场。为了生存,这两个生物体都进化出了独特的策略。宿主利用专门的自噬系统——异噬作用来清除入侵的病原体,而细菌则分泌蛋白质来防御和逃避宿主的异噬作用。已经鉴定出了几种分子,它们的结构研究使我们能够在分子水平上理解这些机制。在这篇综述中,我们集中讨论了宿主自噬和细菌防御的一个例子:自噬受体 NDP52 与糖受体半乳糖凝集素-8 一起,在针对 的自噬机制靶向中起着关键作用;而由 分泌的半胱氨酸蛋白酶 RavZ 会在吞噬体膜上切割 LC3-PE。将讨论这两个例子的结构-功能关系以及未来研究的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/9b83f0632c4b/molce-41-1-27f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/34109d360814/molce-41-1-27f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/370f08216de5/molce-41-1-27f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/9b83f0632c4b/molce-41-1-27f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/34109d360814/molce-41-1-27f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/370f08216de5/molce-41-1-27f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44a9/5792709/9b83f0632c4b/molce-41-1-27f3.jpg

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J Antibiot (Tokyo). 2017 Sep 13;71(1):72-8. doi: 10.1038/ja.2017.104.
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LC3-Associated Phagocytosis and Inflammation.LC3相关吞噬作用与炎症
J Mol Biol. 2017 Nov 24;429(23):3561-3576. doi: 10.1016/j.jmb.2017.08.012. Epub 2017 Aug 25.
3
Monitoring and Measuring Autophagy.监测与测量自噬
Galectin-8N-Selective 4-Halophenylphthalazinone-Galactals Double π-Stack in a Unique Pocket.
半乳糖凝集素-8N-选择性4-卤代苯基酞嗪酮-半乳糖衍生物在独特口袋中的双π堆积。
ACS Med Chem Lett. 2024 Jul 22;15(8):1319-1324. doi: 10.1021/acsmedchemlett.4c00212. eCollection 2024 Aug 8.
4
Harnessing autophagy: A potential breakthrough in digestive disease treatment.利用自噬:消化疾病治疗的潜在突破。
World J Gastroenterol. 2024 Jun 28;30(24):3036-3043. doi: 10.3748/wjg.v30.i24.3036.
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Targeting selective autophagy and beyond: From underlying mechanisms to potential therapies.靶向选择性自噬及其相关研究:从潜在机制到潜在治疗方法。
J Adv Res. 2024 Nov;65:297-327. doi: 10.1016/j.jare.2024.05.009. Epub 2024 May 14.
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Eliminating the invading extracellular and intracellular FnBp bacteria from respiratory epithelial cells by autophagy mediated through FnBp-Fn-Integrin α5β1 axis.通过 FnBp-Fn-整合素 α5β1 轴介导的自噬作用从呼吸上皮细胞中清除入侵的细胞外和细胞内 FnBp 细菌。
Front Cell Infect Microbiol. 2024 Jan 9;13:1324727. doi: 10.3389/fcimb.2023.1324727. eCollection 2023.
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Postbiotics Suppress Infection via Modulating Bacterial Pathogenicity, Autophagy and Inflammasome in Mice.后生元通过调节小鼠的细菌致病性、自噬和炎性小体来抑制感染。
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Modulation of Autophagy and Cell Death by Bacterial Outer-Membrane Vesicles.细菌外膜囊泡对自噬和细胞死亡的调控。
Toxins (Basel). 2023 Aug 14;15(8):502. doi: 10.3390/toxins15080502.
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