G0/G1 arrest and apoptosis induced by SARS-CoV 3b protein in transfected cells.
G0/G1 arrest and apoptosis induced by SARS-CoV 3b protein in transfected cells.
复制标题
SARS-COV 3B蛋白在转染的细胞中诱导的G0/G1停滞和凋亡。
DOI：
10.1186/1743-422x-2-66
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发表时间：
2005-08-17
期刊：
影响因子：
4.8
通讯作者：
Cong Y
中科院分区：
文献类型：
--
作者：
Yuan X;Shan Y;Zhao Z;Chen J;Cong Y
严重急性呼吸综合征冠状病毒（SARS-CoV）是危及生命的非典型肺炎的病因，感染许多器官，如肺、肝和免疫器官，并诱导实质细胞凋亡和坏死。 SARS-CoV 的基因组与之前描述的任何冠状病毒都没有密切关系，它编码复制酶和四种主要结构蛋白以及许多非结构蛋白。已发表的研究表明，一些非结构蛋白可能在病毒的复制、毒力和发病机制中发挥重要作用。在潜在的 SARS-CoV 非结构蛋白中，3b 蛋白 (ORF4) 预计编码 154 个氨基酸，与任何已知蛋白缺乏显着相似性。目前，关于3b蛋白的功能尚未见报道。在本研究中，3b 基因与 C 末端的 EGFP 标签连接。通过细胞周期分析发现，Vero、293和COS-7细胞中过表达3b-EGFP蛋白可诱导细胞周期阻滞于G0/G1期，尤其在COS-7细胞中，转染后24 h开始表达3b-EGFP可诱导亚G1期增加，48 h最为明显。 7-AAD和Annexin V双细胞标记进一步证实了3b融合蛋白对COS-7细胞的凋亡诱导作用，3b蛋白诱导细胞G0/G1期阻滞和凋亡的功能可能为进一步研究SARS发病机制提供新的思路。
Severe Acute Respiratory Syndrome coronavirus (SARS-CoV), cause of the life-threatening atypical pneumonia, infects many organs, such as lung, liver and immune organ, and induces parenchyma cells apoptosis and necrosis. The genome of SARS-CoV, not closely related to any of the previously characterized coronavirus, encodes replicase and four major structural proteins and a number of non-structural proteins. Published studies suggest that some non-structural proteins may play important roles in the replication, virulence and pathogenesis of viruses. Among the potential SARS-CoV non-structural proteins, 3b protein (ORF4) is predicted encoding 154 amino acids, lacking significant similarities to any known proteins. Till now, there is no report about the function of 3b protein. In this study, 3b gene was linked with the EGFP tag at the C- terminus. Through cell cycle analysis, it was found that over-expression of 3b-EGFP protein in Vero, 293 and COS-7 cells could induce cell cycle arrest at G0/G1 phase, and that especially in COS-7 cells, expression of 3b-EGFP was able to induce the increase of sub-G1 phase from 24 h after transfection, which was most obvious at 48 h. The apoptosis induction of 3b fusion protein in COS-7 cells was further confirmed by double cell labeling with 7-AAD and Annexin V, the function of 3b protein inducing cell G0/G1 arrest and apoptosis may provide a new insight for further study on the mechanism of SARS pathogenesis.