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本文引用的文献

1
The interplay of autophagy and β-Catenin signaling regulates differentiation in acute myeloid leukemia.自噬与β-连环蛋白信号传导的相互作用调节急性髓系白血病的分化。
Cell Death Discov. 2015 Sep 21;1:15031. doi: 10.1038/cddiscovery.2015.31. eCollection 2015.
2
Nitric Oxide Interacts with Caveolin-1 to Facilitate Autophagy-Lysosome-Mediated Claudin-5 Degradation in Oxygen-Glucose Deprivation-Treated Endothelial Cells.一氧化氮与小窝蛋白-1相互作用,促进氧糖剥夺处理的内皮细胞中自噬-溶酶体介导的紧密连接蛋白5降解。
Mol Neurobiol. 2016 Nov;53(9):5935-5947. doi: 10.1007/s12035-015-9504-8. Epub 2015 Oct 29.
3
Considering autophagy, β-Catenin and E-Cadherin as innovative therapy aspects in AML.将自噬、β-连环蛋白和E-钙黏蛋白视为急性髓系白血病创新治疗的方向。
Cell Death Dis. 2015 Oct 29;6(10):e1950. doi: 10.1038/cddis.2015.314.
4
Docosahexaenoic Acid Attenuated Experimental Chronic Colitis in Interleukin 10-Deficient Mice by Enhancing Autophagy Through Inhibition of the mTOR Pathway.二十二碳六烯酸通过抑制 mTOR 通路增强自噬来减轻白细胞介素 10 缺陷型小鼠的实验性慢性结肠炎。
JPEN J Parenter Enteral Nutr. 2017 Jul;41(5):824-829. doi: 10.1177/0148607115609308. Epub 2015 Sep 25.
5
Cadherin signaling: keeping cells in touch.钙黏蛋白信号传导:维持细胞间联系。
F1000Res. 2015 Aug 12;4(F1000 Faculty Rev):550. doi: 10.12688/f1000research.6445.1. eCollection 2015.
6
The Selective Degradation of Synaptic Connexin 43 Protein by Hypoxia-induced Autophagy Impairs Natural Killer Cell-mediated Tumor Cell Killing.缺氧诱导的自噬对突触连接蛋白43的选择性降解削弱了自然杀伤细胞介导的肿瘤细胞杀伤作用。
J Biol Chem. 2015 Sep 25;290(39):23670-9. doi: 10.1074/jbc.M115.651547. Epub 2015 Jul 28.
7
Autophagy induction impairs migration and invasion by reversing EMT in glioblastoma cells.自噬诱导通过逆转胶质母细胞瘤细胞中的上皮-间质转化来损害迁移和侵袭能力。
Mol Oncol. 2015 Oct;9(8):1612-25. doi: 10.1016/j.molonc.2015.04.016. Epub 2015 May 13.
8
Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy.CAV1/小窝蛋白-1通过调节溶酶体功能和自噬在人乳腺癌细胞应激反应中的关键作用。
Autophagy. 2015;11(5):769-84. doi: 10.1080/15548627.2015.1034411.
9
Celastrol ameliorates experimental colitis in IL-10 deficient mice via the up-regulation of autophagy.雷公藤红素通过上调自噬改善白细胞介素-10缺陷小鼠的实验性结肠炎。
Int Immunopharmacol. 2015 May;26(1):221-8. doi: 10.1016/j.intimp.2015.03.033. Epub 2015 Apr 6.
10
New cellular mechanisms of gap junction degradation and recycling.间隙连接降解与再循环的新细胞机制。
Biol Cell. 2015 Jul;107(7):218-31. doi: 10.1111/boc.201400048. Epub 2015 May 6.

自噬在上皮细胞连接调节中的作用。

Role of autophagy in the regulation of epithelial cell junctions.

作者信息

Nighot Prashant, Ma Thomas

机构信息

Department of Internal Medicine, University of New Mexico School of Medicine , Albuquerque, NM, USA.

Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM, USA; Veterans Affairs Medical Center, Albuquerque, NM, USA.

出版信息

Tissue Barriers. 2016 Jun 9;4(3):e1171284. doi: 10.1080/21688370.2016.1171284. eCollection 2016 Jul-Sep.

DOI:10.1080/21688370.2016.1171284
PMID:27583189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4993570/
Abstract

Autophagy is a cell survival mechanism by which bulk cytoplasmic material, including soluble macromolecules and organelles, is targeted for lysosomal degradation. The role of autophagy in diverse cellular processes such as metabolic stress, neurodegeneration, cancer, aging, immunity, and inflammatory diseases is being increasingly recognized. Epithelial cell junctions play an integral role in the cell homeostasis via physical binding, regulating paracellular pathways, integrating extracellular cues into intracellular signaling, and cell-cell communication. Recent data indicates that cell junction composition is very dynamic. The junctional protein complexes are actively regulated in response to various intra- and extra-cellular clues by intracellular trafficking and degradation pathways. This review discusses the recent and emerging information on how autophagy regulates various epithelial cell junctions. The knowledge of autophagy regulation of epithelial junctions will provide further rationale for targeting autophagy in a wide variety of human disease conditions.

摘要

自噬是一种细胞存活机制,通过该机制,包括可溶性大分子和细胞器在内的大量细胞质物质被靶向进行溶酶体降解。自噬在多种细胞过程中的作用,如代谢应激、神经退行性变、癌症、衰老、免疫和炎症性疾病,正越来越受到认可。上皮细胞连接通过物理结合、调节细胞旁途径、将细胞外信号整合到细胞内信号传导以及细胞间通讯,在细胞内稳态中发挥不可或缺的作用。最近的数据表明,细胞连接组成非常动态。连接蛋白复合物通过细胞内运输和降解途径,响应各种细胞内和细胞外线索而受到积极调节。本综述讨论了关于自噬如何调节各种上皮细胞连接的最新和新出现的信息。上皮连接自噬调节的知识将为在多种人类疾病情况下靶向自噬提供进一步的理论依据。