开放式参考框架
严重急性呼吸综合征
打开阅读框
转染
冠状病毒
基因
生物
发病机制
病毒学
氨基酸
突变
遗传学
2019年冠状病毒病(COVID-19)
医学
肽序列
免疫学
病理
疾病
传染病(医学专业)
作者
Xiaoling Yuan,Yajun Shan,Zhenyu Yao,Jianyong Li,Zhenhu Zhao,Jiapei Chen,Yuwen Cong
出处
期刊:Molecules and Cells
[Springer Science+Business Media]
日期:2006-04-01
卷期号:21 (2): 186-191
被引量:39
标识
DOI:10.1016/s1016-8478(23)12878-0
摘要
Severe acute respiratory syndrome-associated coronavirus (SARS-CoV), a distant member of the Group 2 coronaviruses, has recently been identified as the etiological agent of severe acute respiratory syndrome (SARS). The genome of SARS-CoV contains four structural genes that are homologous to genes found in other coronaviruses, as well as six subgroup-specific open reading frames (ORFs). ORF3 encodes a predicted 154-amino-acid protein that lacks similarity to any known protein, and is designated 3b in this article. We reported previously that SARS-CoV 3b is predominantly localized in the nucleolus, and induces G0/G1 arrest and apoptosis in transfected cells. In this study, we show that SARS-CoV 3b fused with EGFP at its Nor Cterminus co-localized with a mitochondriaspecific marker in some transfected cells. Mutation analysis of SARS-CoV 3b revealed that the domain spanning amino acids 80 to 138 was essential for its mitochondria localization. These results provide new directions for studies of the role of SARS-CoV 3b protein in SARS pathogenesis.
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