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2
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本文引用的文献

1
The severe acute respiratory syndrome coronavirus 3a is a novel structural protein.严重急性呼吸综合征冠状病毒3a是一种新型结构蛋白。
Biochem Biophys Res Commun. 2005 Apr 29;330(1):286-92. doi: 10.1016/j.bbrc.2005.02.153.
2
Severe acute respiratory syndrome coronavirus 3a protein is a viral structural protein.严重急性呼吸综合征冠状病毒3a蛋白是一种病毒结构蛋白。
J Virol. 2005 Mar;79(5):3182-6. doi: 10.1128/JVI.79.5.3182-3186.2005.
3
Overexpression of 7a, a protein specifically encoded by the severe acute respiratory syndrome coronavirus, induces apoptosis via a caspase-dependent pathway.严重急性呼吸综合征冠状病毒特异性编码的蛋白质7a的过表达通过半胱天冬酶依赖性途径诱导细胞凋亡。
J Virol. 2004 Dec;78(24):14043-7. doi: 10.1128/JVI.78.24.14043-14047.2004.
4
A human in vitro model system for investigating genome-wide host responses to SARS coronavirus infection.一种用于研究全基因组宿主对严重急性呼吸综合征冠状病毒感染反应的体外模型系统。
BMC Infect Dis. 2004 Sep 9;4:34. doi: 10.1186/1471-2334-4-34.
5
Characterization of the 3a protein of SARS-associated coronavirus in infected vero E6 cells and SARS patients.严重急性呼吸综合征相关冠状病毒3a蛋白在感染的非洲绿猴肾细胞E6和严重急性呼吸综合征患者中的特性分析
J Mol Biol. 2004 Jul 30;341(1):271-9. doi: 10.1016/j.jmb.2004.06.016.
6
Pulmonary pathology of severe acute respiratory syndrome in Toronto.多伦多严重急性呼吸综合征的肺部病理学
Mod Pathol. 2005 Jan;18(1):1-10. doi: 10.1038/modpathol.3800247.
7
Regulated de novo biosynthesis of fibrinogen in extrahepatic epithelial cells in response to inflammation.炎症刺激下肝外上皮细胞中纤维蛋白原的调控性从头生物合成。
Thromb Haemost. 2004 Aug;92(2):234-43. doi: 10.1160/TH04-01-0024.
8
Discovery of novel human and animal cells infected by the severe acute respiratory syndrome coronavirus by replication-specific multiplex reverse transcription-PCR.通过复制特异性多重逆转录聚合酶链反应发现感染严重急性呼吸综合征冠状病毒的新型人类和动物细胞
J Clin Microbiol. 2004 Jul;42(7):3196-206. doi: 10.1128/JCM.42.7.3196-3206.2004.
9
A novel severe acute respiratory syndrome coronavirus protein, U274, is transported to the cell surface and undergoes endocytosis.一种新型严重急性呼吸综合征冠状病毒蛋白U274被转运至细胞表面并发生内吞作用。
J Virol. 2004 Jul;78(13):6723-34. doi: 10.1128/JVI.78.13.6723-6734.2004.
10
Identification of a novel protein 3a from severe acute respiratory syndrome coronavirus.从严重急性呼吸综合征冠状病毒中鉴定出一种新型蛋白质3a。
FEBS Lett. 2004 May 7;565(1-3):111-6. doi: 10.1016/j.febslet.2004.03.086.

严重急性呼吸综合征冠状病毒3a蛋白上调肺上皮细胞中纤维蛋白原的表达。

The severe acute respiratory syndrome coronavirus 3a protein up-regulates expression of fibrinogen in lung epithelial cells.

作者信息

Tan Yee-Joo, Tham Puay-Yoke, Chan Daphne Z L, Chou Chih-Fong, Shen Shuo, Fielding Burtram C, Tan Timothy H P, Lim Seng Gee, Hong Wanjin

机构信息

Institute of Molecular and Cell Biology, Proteos, Singapore.

出版信息

J Virol. 2005 Aug;79(15):10083-7. doi: 10.1128/JVI.79.15.10083-10087.2005.

DOI:10.1128/JVI.79.15.10083-10087.2005
PMID:16014971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1181587/
Abstract

Here we analyzed the gene expression profile of cells that stably express the severe acute respiratory syndrome coronavirus (SARS-CoV) 3a protein to determine its effects on host functions. A lung epithelial cell-line, A549, was chosen for this study because the lung is the primary organ infected by SARS-CoV and fatalities resulted mainly from pulmonary complications. Our results showed that the expression of 3a up-regulates the mRNA levels of all three subunits, Aalpha, Bbeta, and gamma, of fibrinogen. Consequently, the intracellular levels as well as the secretion of fibrinogen were increased. We also observed increased fibrinogen levels in SARS-CoV-infected Vero E6 cells.

摘要

在此,我们分析了稳定表达严重急性呼吸综合征冠状病毒(SARS-CoV)3a蛋白的细胞的基因表达谱,以确定其对宿主功能的影响。本研究选用了肺上皮细胞系A549,因为肺是受SARS-CoV感染的主要器官,且死亡主要由肺部并发症导致。我们的结果表明,3a的表达上调了纤维蛋白原的所有三个亚基Aα、Bβ和γ的mRNA水平。因此,纤维蛋白原的细胞内水平以及分泌量均增加。我们还观察到SARS-CoV感染的Vero E6细胞中纤维蛋白原水平升高。