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A critical role of N-myc and STAT interactor (Nmi) in foot-and-mouth disease virus (FMDV) 2C-induced apoptosis

文献类型： 外文期刊

作者： Wang, Jianchang 1 ; Wang, Yongqiang 1 ; Liu, Jue 4 ; Ding, Lin 1 ; Zhang, Quanhong 1 ; Li, Xiaoqi 1 ; Cao, Hong 1 ; Tang, Jun 1 ; Zheng, Shijun J. 1 ;

作者机构： 1.China Agr Univ, Coll Vet Med, Beijing 100193, Peoples R China

2.China Agr Univ, State Key Lab Agrobiotechnol, Beijing 100193, Peoples R China

3.China Agr Univ, Key Lab Zoonosis, Minist Agr, Beijing 100193, Peoples R China

4.Beijing Acad Agr & Forestry, Inst Vet & Anim Sci, Beijing 100097, Peoples R China

关键词： Foot-mouth disease virus (FMDV); N-myc and STAT interactor Nmi; Foot-mouth disease virus 2C; Apoptosis

期刊名称：VIRUS RESEARCH （ 影响因子：3.303； 五年影响因子：3.445 ）

ISSN： 0168-1702

年卷期： 2012 年 170 卷 1-2 期

页码：

收录情况： SCI

摘要： Foot-and-mouth disease virus (FMDV) 2C, is one of the most highly-conserved viral proteins among the serotypes of FMDV. However, its effect on host cells is not very clear. Using yeast two-hybrid system and immunoprecipitation approaches, we found that FMDV 2C interacted with the N-myc and STAT interactor (Nmi) protein. When expressed in cells, FMDV 2C is mainly associated with endoplasmic reticulum in the forms of speckles. In the absence of FMDV 2C, Nmi was distributed diffusely in the cytoplasm. However, upon FMDV 2C overexpression Nmi was recruited into FMDV 2C containing speckles where both proteins are co-localized. In addition, FMDV 2C induced apoptosis in BHK-21 cells, which was markedly inhibited by Nmi knockdown, suggesting that Nmi may play a critical role in FMDV 2C-induced apoptosis. These findings may help to further understand the molecular mechanism of pathogenesis of FMDV infection. (c) 2012 Elsevier B.V. All rights reserved.

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