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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 |
Appears in Collections: | Staff Publications Elements |
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