2. Academic Validation
  3. CK1α upregulates the IFNAR1 expression to prompt the anti-HBV effect of type I IFN in hepatoma carcinoma cells

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

  • Virol Sin. 2022 Aug 17;S1995-820X(22)00143-2. doi: 10.1016/j.virs.2022.08.004.
Jing Xiong 1,  Yanjun Jiang 1,  Jinru Zhang 1,  Yanmeng Chen 1,  Yuan Hu 2
Affiliations

Affiliations

  • 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.
  • 2 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. Electronic address: huyuan@cqmu.edu.cn.
PMID: 35985475 DOI: 10.1016/j.virs.2022.08.004
Abstract

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.

Keywords

Casein kinase 1α (CK1α); Hepatitis B virus (HBV); Interferon-α (IFN-α); Interferon-α/β receptor 1 (IFNAR1).

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