CK1α upregulates the IFNAR1 expression to prompt the anti-HBV effect of type Ⅰ IFN in hepatoma carcinoma cells  

作　　者：Jing Xiong Yanjun Jiang Jinru Zhang Yanmeng Chen Yuan Hu 

机构地区：[1]Key Laboratory of Molecular Biology on Infectious Diseases,Ministry of Education,Institute for Viral Hepatitis,Department of Infectious Diseases,Second Affiliated Hospital,Chongqing Medical University,Chongqing,400016,China

出　　处：《Virologica Sinica》2022年第6期894-903,共10页中国病毒学（英文版）

基　　金：supported by the National Key Research and Development Program of China(2018YFE0107500);the Natural Science Foundation Project of Science and Technology Agency of Chongqing YuZhong District(20200122)to Hu Yuan;a Natural Science Foundation Project of CQ CSTC(cstc2021jcyj-msxmX0276)to Chen YanMeng

摘　　要：Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti-HBV effects of IFN-α are less reported. Here we show that CK1α can interact with IFNAR1 in hepatoma carcinoma cells and increased the abundance of IFNAR1 by reducing the ubiquitination levels in the presence of HBV.Furthermore, CK1α promotes the IFN-α triggered JAK-STAT signaling pathway and consequently enhances the antiviral effects of IFN-α against HBV replication. Our results collectively provide evidence that CK1α positively regulates the anti-HBV activity of IFN-α in hepatoma carcinoma cells, which would be a promising therapeutic target to improve the effectiveness of IFN-α therapy to cure CHB.

关 键 词：Hepatitis B virus(HBV) Casein kinase 1α(CK1α) Interferon-α/βreceptor 1(IFNAR1) Interferon-α(IFN-α) 

分 类 号：R735.7[医药卫生—肿瘤]