坦克结合激酶1
促炎细胞因子
基因敲除
生物
先天免疫系统
小发夹RNA
细胞生物学
RNA干扰
泛素
激酶
磷酸化
NF-κB
核糖核酸
信号转导
免疫系统
免疫学
蛋白激酶A
基因
炎症
MAP激酶激酶激酶
遗传学
作者
Wei Cao,Yifei Guo,Zhikui Cheng,Gang Xu,Qi Zuo,Longyu Nie,Haibin Yu,Ying Zhu
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2021-06-01
卷期号:206 (11): 2668-2681
被引量:3
标识
DOI:10.4049/jimmunol.2001262
摘要
Abstract The antiviral innate immune responses are crucial steps during host defense and must be strictly regulated, but the molecular mechanisms of control remain unclear. In this study, we report increased expression of human ATPase Na+/K+ transporting subunit β 1(ATP1B1) after DNA and RNA virus infections. We found that the expression of ATP1B1 can inhibit viral replication and increase the levels of IFNs, IFN-stimulated genes, and inflammatory cytokines. Knockdown of ATP1B1 by specific short hairpin RNA had the opposite effects. Upon viral infection, ATP1B1 was induced, interacted with TRAF3 and TRAF6, and potentiated the ubiquitination of these proteins, leading to increased phosphorylation of downstream molecules, including TGF-β–activated kinase 1 (TAK1) and TANK-binding kinase 1 (TBK1). These results reveal a previously unrecognized role of ATP1B1 in antiviral innate immunity and suggest a novel mechanism for the induction of IFNs and proinflammatory cytokines during viral infection.
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