Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells
DC Field | Value | Language |
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dc.contributor.author | Choi, Eun-Jin | - |
dc.contributor.author | Kim, Sewoon | - |
dc.contributor.author | Jho, Eek-hoon | - |
dc.contributor.author | Song, Ki-Joon | - |
dc.contributor.author | Kee, Sun-Ho | - |
dc.date.accessioned | 2021-09-06T00:18:42Z | - |
dc.date.available | 2021-09-06T00:18:42Z | - |
dc.date.created | 2021-06-14 | - |
dc.date.issued | 2013-07 | - |
dc.identifier.issn | 0022-1317 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/102869 | - |
dc.description.abstract | Herpes simplex virus type 1 (HSV-1) replicates in various cell types and induces early cell death, which limits viral replication in certain cell types. Axin is a scaffolding protein that regulates Wnt signalling and participates in various cellular events, including cellular proliferation and cell death. The effects of axin expression on HSV-1 infection were investigated based on our initial observation that Wnt3a treatment or axin knockdown reduced HSV-1 replication. L929 cells expressed the axin protein in a doxycycline-inducible manner (L-axin) and enhanced HSV-1 replication in comparison to control cells (L-EV). HSV-1 infection induced cell death as early as 6 h after infection through the necrotic pathway and required de novo protein synthesis in L929 cells. Subsequent analysis of viral protein expression suggested that axin expression led to suppression of HSV-1-induced premature cell death, resulting in increased late gene expression. In analysis of axin deletion mutants, the regulators of the G-protein signalling (RGS) domain were involved in the axin-mediated enhancement of viral replication and reduction in cell death. These results suggest that viral replication enhancement might be mediated by the axin RGS domain. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | SOC GENERAL MICROBIOLOGY | - |
dc.subject | ADENOMATOUS POLYPOSIS-COLI | - |
dc.subject | WNT SIGNALING PATHWAY | - |
dc.subject | BETA-CATENIN | - |
dc.subject | MUTANT HUNTINGTIN | - |
dc.subject | INDUCED NECROPTOSIS | - |
dc.subject | JNK ACTIVATION | - |
dc.subject | PROTEIN | - |
dc.subject | APOPTOSIS | - |
dc.subject | APC | - |
dc.subject | AUTOPHAGY | - |
dc.title | Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Song, Ki-Joon | - |
dc.contributor.affiliatedAuthor | Kee, Sun-Ho | - |
dc.identifier.doi | 10.1099/vir.0.051540-0 | - |
dc.identifier.scopusid | 2-s2.0-84879145041 | - |
dc.identifier.wosid | 000322855900021 | - |
dc.identifier.bibliographicCitation | JOURNAL OF GENERAL VIROLOGY, v.94, pp.1636 - 1646 | - |
dc.relation.isPartOf | JOURNAL OF GENERAL VIROLOGY | - |
dc.citation.title | JOURNAL OF GENERAL VIROLOGY | - |
dc.citation.volume | 94 | - |
dc.citation.startPage | 1636 | - |
dc.citation.endPage | 1646 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biotechnology & Applied Microbiology | - |
dc.relation.journalResearchArea | Virology | - |
dc.relation.journalWebOfScienceCategory | Biotechnology & Applied Microbiology | - |
dc.relation.journalWebOfScienceCategory | Virology | - |
dc.subject.keywordPlus | ADENOMATOUS POLYPOSIS-COLI | - |
dc.subject.keywordPlus | WNT SIGNALING PATHWAY | - |
dc.subject.keywordPlus | BETA-CATENIN | - |
dc.subject.keywordPlus | MUTANT HUNTINGTIN | - |
dc.subject.keywordPlus | INDUCED NECROPTOSIS | - |
dc.subject.keywordPlus | JNK ACTIVATION | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | APC | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
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