小鼠冠状病毒感染的培养细胞中凋亡的诱导以及E蛋白作为凋亡诱导剂的证明。
Induction of apoptosis in murine coronavirus-infected cultured cells and demonstration of E protein as an apoptosis inducer.
作者信息
An S, Chen C J, Yu X, Leibowitz J L, Makino S
机构信息
Department of Microbiology and Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA.
出版信息
J Virol. 1999 Sep;73(9):7853-9. doi: 10.1128/JVI.73.9.7853-7859.1999.
Abstract
We demonstrated that infection of 17Cl-1 cells with the murine coronavirus mouse hepatitis virus (MHV) induced caspase-dependent apoptosis. MHV-infected DBT cells did not show apoptotic changes, indicating that apoptosis was not a universal mechanism of cell death in MHV-infected cells. Expression of MHV structural proteins by recombinant vaccinia viruses showed that expression of MHV E protein induced apoptosis in DBT cells, whereas expression of other MHV structural proteins, including S protein, M protein, N protein, and hemagglutinin-esterase protein, failed to induce apoptosis. MHV E protein-mediated apoptosis was suppressed by a high level of Bcl-2 oncogene expression. Our data showed that MHV E protein is a multifunctional protein; in addition to its known function in coronavirus envelope formation, it also induces apoptosis.
摘要
我们证明，用鼠冠状病毒小鼠肝炎病毒（MHV）感染17Cl-1细胞可诱导半胱天冬酶依赖性凋亡。感染MHV的DBT细胞未显示凋亡变化，这表明凋亡并非MHV感染细胞中细胞死亡的普遍机制。重组痘苗病毒对MHV结构蛋白的表达显示，MHV E蛋白的表达可诱导DBT细胞凋亡，而其他MHV结构蛋白，包括S蛋白、M蛋白、N蛋白和血凝素酯酶蛋白的表达则未能诱导凋亡。高水平的Bcl-2癌基因表达可抑制MHV E蛋白介导的凋亡。我们的数据表明，MHV E蛋白是一种多功能蛋白；除了其在冠状病毒包膜形成中的已知功能外，它还可诱导凋亡。
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