Please use this identifier to cite or link to this item: https://doi.org/10.1155/2016/7425628
Title: HCV-Induced Oxidative Stress: Battlefield-Winning Strategy
Authors: Rebbani, K 
Tsukiyama-Kohara, K
Keywords: Acetylation
Cytology
Enzyme activity
Machinery
Viruses
Chronic infection
Hepatitis C virus
Hepatocarcinogenesis
Immune response
Lipid metabolisms
Liver disease
Winning strategy
Oxidative stress
3beta hydroxysterol delta24 reductase
oxidoreductase
unclassified drug
antioxidant
antivirus agent
biological marker
DHCR24 protein, human
MDM2 protein, human
nerve protein
oxidoreductase
protein MDM2
protein p53
TP53 protein, human
dendritic cell
endoplasmic reticulum
Hepatitis B virus
hepatitis C
Hepatitis C virus
human
liver cell carcinoma
nonhuman
oxidative stress
Review
stellate cell
acetylation
animal
complication
drug effects
Hepacivirus
Hepatitis C, Chronic
host pathogen interaction
liver tumor
metabolism
pathogenicity
protein degradation
signal transduction
virology
Acetylation
Animals
Antioxidants
Antiviral Agents
Biomarkers
Carcinoma, Hepatocellular
Hepacivirus
Hepatitis C, Chronic
Host-Pathogen Interactions
Humans
Liver Neoplasms
Nerve Tissue Proteins
Oxidative Stress
Oxidoreductases Acting on CH-CH Group Donors
Proteolysis
Proto-Oncogene Proteins c-mdm2
Signal Transduction
Tumor Suppressor Protein p53
Issue Date: 2016
Citation: Rebbani, K, Tsukiyama-Kohara, K (2016). HCV-Induced Oxidative Stress: Battlefield-Winning Strategy. Oxidative Medicine and Cellular Longevity 2016 : 7425628. ScholarBank@NUS Repository. https://doi.org/10.1155/2016/7425628
Rights: Attribution 4.0 International
Abstract: About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. © 2016 Khadija Rebbani and Kyoko Tsukiyama-Kohara.
Source Title: Oxidative Medicine and Cellular Longevity
URI: https://scholarbank.nus.edu.sg/handle/10635/179979
ISSN: 19420900
DOI: 10.1155/2016/7425628
Rights: Attribution 4.0 International
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