Hepatitis C Virus NS2 Protein Inhibits DNA Damage Pathway by Sequestering p53 to the Cytoplasm

dc.contributor.authorBittar, Cintia [UNESP]
dc.contributor.authorShrivastava, Shubham
dc.contributor.authorBhanja Chowdhury, Joydip
dc.contributor.authorRahal, Paula [UNESP]
dc.contributor.authorRay, Ratna B.
dc.contributor.institutionSaint Louis University
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:29:00Z
dc.date.available2014-05-27T11:29:00Z
dc.date.issued2013-04-30
dc.description.abstractChronic hepatitis C virus (HCV) infection is an important cause of morbidity and mortality globally, and often leads to end-stage liver disease. The DNA damage checkpoint pathway induces cell cycle arrest for repairing DNA in response to DNA damage. HCV infection has been involved in this pathway. In this study, we assess the effects of HCV NS2 on DNA damage checkpoint pathway. We have observed that HCV NS2 induces ataxia-telangiectasia mutated checkpoint pathway by inducing Chk2, however, fails to activate the subsequent downstream pathway. Further study suggested that p53 is retained in the cytoplasm of HCV NS2 expressing cells, and p21 expression is not enhanced. We further observed that HCV NS2 expressing cells induce cyclin E expression and promote cell growth. Together these results suggested that HCV NS2 inhibits DNA damage response by altering the localization of p53, and may play a role in the pathogenesis of HCV infection. © 2013 Bitter et al.en
dc.description.affiliationDepartment of Pathology Saint Louis University, St. Louis, MO
dc.description.affiliationDeaprtment of Biology UNESP - São Paulo State University, São José do Rio Preto, São Paulo
dc.description.affiliationUnespDeaprtment of Biology UNESP - São Paulo State University, São José do Rio Preto, São Paulo
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0062581
dc.identifier.citationPLoS ONE, v. 8, n. 4, 2013.
dc.identifier.doi10.1371/journal.pone.0062581
dc.identifier.file2-s2.0-84876964411.pdf
dc.identifier.issn1932-6203
dc.identifier.lattes7991082362671212
dc.identifier.orcid0000-0001-5693-6148
dc.identifier.scopus2-s2.0-84876964411
dc.identifier.urihttp://hdl.handle.net/11449/75191
dc.identifier.wosWOS:000319077300077
dc.language.isoeng
dc.relation.ispartofPLOS ONE
dc.relation.ispartofjcr2.766
dc.relation.ispartofsjr1,164
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjectcheckpoint kinase 2
dc.subjectcyclin E
dc.subjectnonstructural protein 2
dc.subjectprotein p21
dc.subjectprotein p53
dc.subjectcell growth
dc.subjectcell proliferation
dc.subjectcontrolled study
dc.subjectcytoplasm
dc.subjectDNA damage
dc.subjectHepatitis C virus
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectprotein transport
dc.titleHepatitis C Virus NS2 Protein Inhibits DNA Damage Pathway by Sequestering p53 to the Cytoplasmen
dc.typeArtigo
dcterms.licensehttp://www.plos.org/open-access/
unesp.author.lattes7991082362671212[4]
unesp.author.orcid0000-0001-5693-6148[4]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências Letras e Ciências Exatas, São José do Rio Pretopt

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