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严重急性呼吸综合征相关冠状病毒的3a蛋白可诱导Vero E6细胞凋亡。

The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells.

作者信息

Law Patrick T W, Wong Chi-Hang, Au Thomas C C, Chuck Chi-Pang, Kong Siu-Kai, Chan Paul K S, To Ka-Fai, Lo Anthony W I, Chan Judy Y W, Suen Yick-Keung, Chan H Y Edwin, Fung Kwok-Pui, Waye Mary M Y, Sung Joseph J Y, Lo Y M Dennis, Tsui Stephen K W

机构信息

Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.

Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.

出版信息

J Gen Virol. 2005 Jul;86(Pt 7):1921-1930. doi: 10.1099/vir.0.80813-0.

Abstract

An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.

摘要

严重急性呼吸综合征(SARS)疫情在中国爆发,首例病例于2002年11月中旬出现。该疾病的病原体被发现是一种此前未知的冠状病毒,即严重急性呼吸综合征相关冠状病毒(SARS-CoV)。SARS-CoV感染的详细病理学以及宿主对病毒感染的反应仍不清楚。3a基因编码一种非结构病毒蛋白,预计为跨膜蛋白。在本研究中,结果表明3a蛋白在SARS患者的肺和肠道组织中表达,并且该蛋白在转染3a的猴肾Vero E6细胞中定位于内质网。染色质浓缩和DNA片段化的体外实验表明,3a蛋白可能触发细胞凋亡。这些数据表明,单一SARS-CoV蛋白的过表达可在体外诱导细胞凋亡。

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