期刊
JOURNAL OF VIROLOGY
卷 89, 期 3, 页码 1879-1888出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.03079-14
关键词
-
类别
资金
- Funding Program for Next Generation World-Leading Researchers
- Japan Society for the Promotion of Science (JSPS)
- Japan Initiative for Global Research Network on Infectious Diseases (J-GRID)
- Ministry of Education, Culture, Science, Sports and Technology (MEXT) of Japan
- Takeda Science Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Sumitomo Foundation
- Ichiro Kanehara Foundation
- Grants-in-Aid for Scientific Research [26293102] Funding Source: KAKEN
Nonmuscle myosin heavy chain IIA (NMHC-IIA) has been reported to function as a herpes simplex virus 1 (HSV-1) entry coreceptor by interacting with viral envelope glycoprotein B (gB). Vertebrates have three genetically distinct isoforms of the NMHCII, designated NMHC-IIA, NMHC-IIB, and NMHC-IIC. COS cells, which are readily infected by HSV-1, do not express NMHC-IIA but do express NMHC-IIB. This observation prompted us to investigate whether NMHC-IIB might associate with HSV-1 gB and be involved in an HSV-1 entry like NMHC-IIA. In these studies, we show that (i) NMHC-IIB coprecipitated with gB in COS-1 cells upon HSV-1 entry; (ii) a specific inhibitor of myosin light chain kinase inhibited cell surface expression of NMHC-IIB in COS-1 cells upon HSV-1 entry as well as HSV-1 infection, as reported with NMHC-IIA; (iii) overexpression of mouse NMHC-IIB in IC21 cells significantly increased their susceptibility to HSV-1 infection; and (iv) knockdown of NMHC-IIB in COS-1 cells inhibited HSV-1 infection as well as cell-cell fusion mediated by HSV-1 envelope glycoproteins. These results supported the hypothesis that, like NMHC-IIA, NMHC-IIB associated with HSV-1 gB and mediated HSV-1 entry.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据