传染性法氏囊病
亮氨酸拉链
干扰素
生物
泛素
病毒
病毒学
ATF3
细胞生物学
转录因子
基因表达
基因
毒力
生物化学
发起人
作者
Zhiyuan He,Xiang Chen,Mengjiao Fu,Jun Tang,Xiaoqi Li,Hong Cao,Yongqiang Wang,Shijun J. Zheng
出处
期刊:Immunobiology
[Elsevier]
日期:2018-04-01
卷期号:223 (4-5): 374-382
被引量:14
标识
DOI:10.1016/j.imbio.2017.10.048
摘要
Viruses have developed a variety of methods to evade host immune response. Our previous study showed that infectious bursal disease virus (IBDV) inhibited type I interferon production via interaction of VP4 with cellular glucocorticoid-induced leucine zipper (GILZ) protein. However, the exact underlying molecular mechanism is still unclear. In this study, we found that IBDV VP4 suppressed GILZ degradation by inhibiting K48-linked ubiquitylation of GILZ. Furthermore, mutation of VP4 (R41G) abolished the inhibitory effect of VP4 on IFN-β expression and GILZ ubiquitylation, indicating that the amino acid 41R of VP4 was required for the suppression of IFN-β expression and GILZ ubiquitylation. Moreover, IBDV infection or VP4 expression markedly inhibited endogenous GILZ ubiquitylation. Thus, IBDV VP4 suppresses type I interferon expression by inhibiting K48-linked ubiquitylation of GILZ, revealing a new mechanism employed by IBDV to suppress host response.
科研通智能强力驱动
Strongly Powered by AbleSci AI