國家衛生研究院 NHRI:Item 3990099045/10166
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    題名: Pegylated IFN-alpha suppresses hepatitis C virus by promoting the DAPK-mTOR pathway
    其他題名: Pegylated IFN-α suppresses hepatitis C virus by promoting the DAPK-mTOR pathway
    作者: Liu, WL;Yang, HC;Hsu, CS;Wang, CC;Wang, TS;Kao, JH;Chen, DS
    貢獻者: National Mosquito-Borne Diseases Control Research Center
    摘要: Death-associated protein kinase (DAPK) has been found to be induced by IFN, but its antiviral activity remains elusive. Therefore, we investigated whether DAPK plays a role in the pegylated IFN-alpha (peg-IFN-alpha)-induced antiviral activity against hepatitis C virus (HCV) replication. Primary human hepatocytes, Huh-7, and infectious HCV cell culture were used to study the relationship between peg-IFN-alpha and the DAPK-mammalian target of rapamycin (mTOR) pathways. The activation of DAPK and signaling pathways were determined using immunoblotting. By silencing DAPK and mTOR, we further assessed the role of DAPK and mTOR in the peg-IFN-alpha-induced suppression of HCV replication. Peg-IFN-alpha up-regulated the expression of DAPK and mTOR, which was associated with the suppression of HCV replication. Overexpression of DAPK enhanced mTOR expression and then inhibited HCV replication. In addition, knockdown of DAPK reduced the expression of mTOR in peg-IFN-alpha-treated cells, whereas silencing of mTOR had no effect on DAPK expression, suggesting mTOR may be a downstream effector of DAPK. More importantly, knockdown of DAPK or mTOR significantly mitigated the inhibitory effects of peg-IFN-alpha on HCV replication. In conclusion, our data suggest that the DAPK-mTOR pathway is critical for anti-HCV effects of peg-IFN-alpha.
    日期: 2016-12-20
    關聯: Proceedings of the National Academy of Sciences of the United States of America. 2016 Dec 20;113(51):14799-14804.
    Link to: http://dx.doi.org/10.1073/pnas.1618517114
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0027-8424&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000390044900073
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85006459577
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