Please use this identifier to cite or link to this item: https://doi.org/10.1155/2016/7425628
DC FieldValue
dc.titleHCV-Induced Oxidative Stress: Battlefield-Winning Strategy
dc.contributor.authorRebbani, K
dc.contributor.authorTsukiyama-Kohara, K
dc.date.accessioned2020-10-26T05:21:50Z
dc.date.available2020-10-26T05:21:50Z
dc.date.issued2016
dc.identifier.citationRebbani, 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
dc.identifier.issn19420900
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/179979
dc.description.abstractAbout 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectAcetylation
dc.subjectCytology
dc.subjectEnzyme activity
dc.subjectMachinery
dc.subjectViruses
dc.subjectChronic infection
dc.subjectHepatitis C virus
dc.subjectHepatocarcinogenesis
dc.subjectImmune response
dc.subjectLipid metabolisms
dc.subjectLiver disease
dc.subjectWinning strategy
dc.subjectOxidative stress
dc.subject3beta hydroxysterol delta24 reductase
dc.subjectoxidoreductase
dc.subjectunclassified drug
dc.subjectantioxidant
dc.subjectantivirus agent
dc.subjectbiological marker
dc.subjectDHCR24 protein, human
dc.subjectMDM2 protein, human
dc.subjectnerve protein
dc.subjectoxidoreductase
dc.subjectprotein MDM2
dc.subjectprotein p53
dc.subjectTP53 protein, human
dc.subjectdendritic cell
dc.subjectendoplasmic reticulum
dc.subjectHepatitis B virus
dc.subjecthepatitis C
dc.subjectHepatitis C virus
dc.subjecthuman
dc.subjectliver cell carcinoma
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectReview
dc.subjectstellate cell
dc.subjectacetylation
dc.subjectanimal
dc.subjectcomplication
dc.subjectdrug effects
dc.subjectHepacivirus
dc.subjectHepatitis C, Chronic
dc.subjecthost pathogen interaction
dc.subjectliver tumor
dc.subjectmetabolism
dc.subjectpathogenicity
dc.subjectprotein degradation
dc.subjectsignal transduction
dc.subjectvirology
dc.subjectAcetylation
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectAntiviral Agents
dc.subjectBiomarkers
dc.subjectCarcinoma, Hepatocellular
dc.subjectHepacivirus
dc.subjectHepatitis C, Chronic
dc.subjectHost-Pathogen Interactions
dc.subjectHumans
dc.subjectLiver Neoplasms
dc.subjectNerve Tissue Proteins
dc.subjectOxidative Stress
dc.subjectOxidoreductases Acting on CH-CH Group Donors
dc.subjectProteolysis
dc.subjectProto-Oncogene Proteins c-mdm2
dc.subjectSignal Transduction
dc.subjectTumor Suppressor Protein p53
dc.typeReview
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1155/2016/7425628
dc.description.sourcetitleOxidative Medicine and Cellular Longevity
dc.description.volume2016
dc.description.page7425628
dc.published.statePublished
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