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。
Overexpression of 7a, a protein specifically encoded by the severe acute respiratory syndrome coronavirus, induces apoptosis via a caspase-dependent pathway.
作者信息
Tan Yee-Joo, Fielding Burtram C, Goh Phuay-Yee, Shen Shuo, 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. 2004 Dec;78(24):14043-7. doi: 10.1128/JVI.78.24.14043-14047.2004.
Abstract
Besides genes that are homologous to proteins found in other coronaviruses, the severe acute respiratory syndrome coronavirus genome also contains nine other potential open reading frames. Previously, we have characterized the expression and cellular localization of two of these "accessory" viral proteins, 3a (previously termed U274) and 7a (previously termed U122). In this study, we further examined whether they can induce apoptosis, which has been observed clinically. We showed that the overexpression of 7a, but not of 3a or the viral structural proteins, nucleocapsid, membrane, and envelope, induces apoptosis. 7a induces apoptosis via a caspase-dependent pathway and in cell lines derived from different organs, including lung, kidney, and liver.
摘要
除了与其他冠状病毒中发现的蛋白质同源的基因外，严重急性呼吸综合征冠状病毒基因组还包含另外九个潜在的开放阅读框。此前，我们已经对其中两种“辅助”病毒蛋白3a（以前称为U274）和7a（以前称为U122）的表达和细胞定位进行了表征。在本研究中，我们进一步研究了它们是否能诱导临床上已观察到的细胞凋亡。我们发现，7a的过表达可诱导细胞凋亡，而3a或病毒结构蛋白核衣壳、膜和包膜的过表达则不能。7a通过半胱天冬酶依赖性途径在源自不同器官（包括肺、肾和肝）的细胞系中诱导细胞凋亡。
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