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本文引用的文献

1
HIV-1 infection of macrophages induces retention of cholesterol transporter ABCA1 in the endoplasmic reticulum.HIV-1对巨噬细胞的感染会导致胆固醇转运蛋白ABCA1滞留在内质网中。
AIDS Res Hum Retroviruses. 2014 Oct;30(10):947-8. doi: 10.1089/aid.2014.0156. Epub 2014 Sep 8.
2
HIV-1 protein Nef inhibits activity of ATP-binding cassette transporter A1 by targeting endoplasmic reticulum chaperone calnexin.HIV-1病毒蛋白Nef通过靶向内质网伴侣钙连蛋白来抑制ATP结合盒转运体A1的活性。
J Biol Chem. 2014 Oct 17;289(42):28870-84. doi: 10.1074/jbc.M114.583591. Epub 2014 Aug 28.
3
HIV protein Nef causes dyslipidemia and formation of foam cells in mouse models of atherosclerosis.HIV 蛋白 Nef 导致动脉粥样硬化小鼠模型中的血脂异常和泡沫细胞形成。
FASEB J. 2014 Jul;28(7):2828-39. doi: 10.1096/fj.13-246876. Epub 2014 Mar 18.
4
HIV-1 Nef mobilizes lipid rafts in macrophages through a pathway that competes with ABCA1-dependent cholesterol efflux.HIV-1 Nef 通过与 ABCA1 依赖性胆固醇外排竞争的途径在巨噬细胞中动员脂筏。
J Lipid Res. 2012 Apr;53(4):696-708. doi: 10.1194/jlr.M023119. Epub 2012 Jan 19.
5
Circulating Nef induces dyslipidemia in simian immunodeficiency virus-infected macaques by suppressing cholesterol efflux.循环 Nef 通过抑制胆固醇外排诱导感染猴免疫缺陷病毒的猕猴发生血脂异常。
J Infect Dis. 2010 Aug 15;202(4):614-23. doi: 10.1086/654817.
6
The macrophage: the intersection between HIV infection and atherosclerosis.巨噬细胞:HIV 感染与动脉粥样硬化的交汇点。
J Leukoc Biol. 2010 Apr;87(4):589-98. doi: 10.1189/jlb.0809580. Epub 2009 Dec 1.
7
Lipids and membrane microdomains in HIV-1 replication.HIV-1复制中的脂质与膜微结构域
Virus Res. 2009 Aug;143(2):162-76. doi: 10.1016/j.virusres.2009.04.007. Epub 2009 Apr 19.
8
Increased lipid rafts and accelerated lipopolysaccharide-induced tumor necrosis factor-alpha secretion in Abca1-deficient macrophages.Abca1基因缺陷型巨噬细胞中脂筏增加及脂多糖诱导的肿瘤坏死因子-α分泌加速
J Lipid Res. 2007 Feb;48(2):299-306. doi: 10.1194/jlr.M600428-JLR200. Epub 2006 Nov 1.
9
ATP-binding cassette transporter A1 expression disrupts raft membrane microdomains through its ATPase-related functions.ATP结合盒转运蛋白A1的表达通过其与ATP酶相关的功能破坏筏膜微结构域。
J Biol Chem. 2006 Nov 24;281(47):36091-101. doi: 10.1074/jbc.M602247200. Epub 2006 Sep 19.
10
Plasma membrane rafts play a critical role in HIV-1 assembly and release.质膜筏在HIV-1的组装和释放过程中发挥着关键作用。
Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13925-30. doi: 10.1073/pnas.241320298.

HIV感染细胞中ABCA1与胆固醇流出的分析

Analysis of ABCA1 and Cholesterol Efflux in HIV-Infected Cells.

作者信息

Mukhamedova Nigora, Brichacek Beda, Darwish Christina, Popratiloff Anastas, Sviridov Dmitri, Bukrinsky Michael

机构信息

Baker IDI Heart and Diabetes Institute, Melbourne, VIC, 3004, Australia.

Department of Microbiology, Immunology and Tropical Medicine, George Washington University School of Medicine and Health Sciences, Ross Hall, Room 624, 2300 Eye Street, N.W., Washington, DC, 20037, USA.

出版信息

Methods Mol Biol. 2016;1354:281-92. doi: 10.1007/978-1-4939-3046-3_19.

DOI:10.1007/978-1-4939-3046-3_19
PMID:26714719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5047010/
Abstract

Cholesterol is an essential component of the cellular membranes and, by extension, of the HIV envelope membrane, which is derived from the host cell plasma membrane. Depletion of the cellular cholesterol has an inhibitory effect on HIV assembly, reduces infectivity of the produced virions, and makes the cell less susceptible to HIV infection. It is not surprising that the virus has evolved to gain access to cellular proteins regulating cholesterol metabolism. One of the key mechanisms used by HIV to maintain high levels of cholesterol in infected cells is Nef-mediated inhibition of cholesterol efflux and the cholesterol transporter responsible for this process, ABCA1. In this chapter, we describe methods to investigate these effects of HIV-1 infection.

摘要

胆固醇是细胞膜的重要组成部分,进而也是HIV包膜的重要组成部分,HIV包膜源自宿主细胞质膜。细胞内胆固醇的消耗对HIV组装具有抑制作用,降低所产生病毒颗粒的感染性,并使细胞对HIV感染的敏感性降低。病毒进化出获取调节胆固醇代谢的细胞蛋白的能力也就不足为奇了。HIV在受感染细胞中维持高水平胆固醇的关键机制之一是Nef介导的对胆固醇外流及负责此过程的胆固醇转运蛋白ABCA1的抑制作用。在本章中,我们描述了研究HIV-1感染这些效应的方法。