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dc.contributor.authorSmith, Miles Christian
dc.contributor.authorBoutell, Chris
dc.contributor.authorDavido, David J.
dc.date.accessioned2017-03-09T22:04:42Z
dc.date.available2017-03-09T22:04:42Z
dc.date.issued2012-02-01
dc.identifier.citationSmith, Miles C., Chris Boutell, and David J. Davido. "HSV-1 ICP0: Paving the Way for Viral Replication." Future Virology 6.4 (2011): 421-29.en_US
dc.identifier.urihttp://hdl.handle.net/1808/23396
dc.description.abstractHerpes simplex virus type 1 (HSV-1) has two distinct phases of its viral life cycle: lytic and latent. One viral immediate-early protein that is responsible for determining the balance between productive lytic replication and reactivation from latency is infected cell protein 0 (ICP0). ICP0 is a 775-amino acid really interesting new gene (RING)-finger-containing protein that possesses E3 ubiquitin ligase activity, which is required for ICP0 to activate HSV-1 gene expression, disrupt nuclear domain (ND) 10 structures, mediate the degradation of cellular proteins, and evade the host cell’s intrinsic and innate antiviral defenses. This article examines our current understanding of ICP0’s transactivating, E3 ubiquitin ligase, and antihost defense activities and their inter-relationships to one another. Lastly, we will discuss how these properties of ICP0 may be utilized as possible targets for HSV-1 antiviral therapies.en_US
dc.publisherFuture Medicineen_US
dc.subjectE3 ubiquitin ligaseen_US
dc.subjectHerpes simplex virusen_US
dc.subjectICP0en_US
dc.subjectInnate immunityen_US
dc.subjectIntrinsic defenseen_US
dc.subjectNuclear domain 10en_US
dc.subjectViral transactivatoren_US
dc.titleHSV-1 ICP0: paving the way for viral replicationen_US
dc.typeArticleen_US
kusw.kuauthorDavido, David J.
kusw.kudepartmentMolecular Biosciencesen_US
dc.identifier.doi10.2217/fvl.11.24en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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