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Activity‐based profiling of the proteasome pathway during hepatitis C virus infection
Author(s) -
Nasheri Neda,
Ning Zhibin,
Figeys Daniel,
Yao Shao,
Goto Natalie K.,
Pezacki John Paul
Publication year - 2015
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201500169
Subject(s) - proteasome , hepatitis c virus , hepatocellular carcinoma , downregulation and upregulation , ubiquitin , cirrhosis , biology , virology , virus , viral replication , hepacivirus , hepatitis c , immunology , cancer research , medicine , microbiology and biotechnology , biochemistry , gene
Hepatitis C virus (HCV) infection often leads to chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The stability of the HCV proteins is controlled by ubiquitin‐dependent and ubiquitin‐independent proteasome pathways. Many viruses modulate proteasome function for their propagation. To examine the interrelationship between HCV and the proteasome pathways we employed a quantitative activity‐based protein profiling method. Using this approach we were able to quantify the changes in the activity of several proteasome subunits and found that proteasome activity is drastically reduced by HCV replication. The results imply a link between the direct downregulation of the activity of this pathway and chronic HCV infection.