A critical role of interferon-induced protein IFP35 in the type I interferon response in cells induced by foot-and-mouth disease virus (FMDV) protein 2C
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- 作者：Wei Zheng (1) (2) (3) (4)
Xiaying Li (2) (3) (4)
Jianchang Wang (2) (3) (4)
Xiaoqi Li (2) (3) (4)
Hong Cao (2) (3) (4)
Yongqiang Wang (2) (3) (4)
Qinghua Zeng (1)
Shijun J. Zheng (2) (3) (4) - 刊名：Archives of Virology
- 出版年：2014
- 出版时间：November 2014
- 年：2014
- 卷：159
- 期：11
- 页码：2925-2935
- 全文大小：1,393 KB
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Xiaying Li (2) (3) (4)
Jianchang Wang (2) (3) (4)
Xiaoqi Li (2) (3) (4)
Hong Cao (2) (3) (4)
Yongqiang Wang (2) (3) (4)
Qinghua Zeng (1)
Shijun J. Zheng (2) (3) (4)
1. The Laboratory of Molecule and Cellular Physiology, School of Life Sciences, Northeast Normal University, Changchun, 130024, Jilin, China
2. State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing, 100193, China
3. Key Laboratory of Zoonosis of Ministry of Agriculture, China Agricultural University, Beijing, 100193, China
4. College of Veterinary Medicine, China Agricultural University, 2 Yuan-Ming-Yuan West Road, Beijing, 100193, China - ISSN：1432-8798
文摘
Foot-and-mouth disease virus (FMDV) protein 2C is one of the most highly conserved viral proteins among the serotypes of FMDV. However, its effect on host cell response is not very clear. In our previous report, we showed that FMDV protein 2C interacts with cellular protein N-myc and STAT interactor (Nmi), inducing moderate apoptosis in cells. Here, we show that transfection of HEK293T cells with pEGFP-N1-2C or pEGFP-N1-Nmi induces activation of type I interferon promoters, leading to delayed vesicular stomatitis virus (VSV) growth. Using immunoprecipitation and confocal microscopy assays, we found that interferon-induced protein IFP35 interacts with Nmi. Knockdown of IFP35 expression by siRNA abolished pEGFP-N1-2C and pEGFP-N1-Nmi-induced activation of type I interferon promoters and restored VSV growth, suggesting that IFP35 plays a critical role in the type I interferon response induced by FMDV protein 2C. These findings may help to further understand cell responses to FMDV infection.