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dc.contributor.authorHaenchen, Steve D.
dc.contributor.authorUtter, Jeff A.
dc.contributor.authorBayless, Adam M.
dc.contributor.authorDobrowsky, Rick T.
dc.contributor.authorDavido, David J.
dc.date.accessioned2017-05-24T18:35:07Z
dc.date.available2017-05-24T18:35:07Z
dc.date.issued2013-10
dc.identifier.citationHaenchen, S.D., Utter, J.A., Bayless, A.M. et al. Journal of NeuroVirology (2010) 16: 405. doi:10.3109/13550284.2010.513030en_US
dc.identifier.urihttp://hdl.handle.net/1808/24302
dc.description.abstractPrevious studies have shown that herpes simplex virus type 1 (HSV-1) replication is inhibited by the cyclin-dependent kinase (cdk) inhibitor roscovitine. One roscovitine-sensitive cdk that functions in neurons is cdk5, which is activated in part by its binding partner, p35. Because HSV establishes latent infections in sensory neurons, we sought to determine the role p35 plays in HSV-1 replication in vivo. For these studies, wild-type (wt) and p35-/- mice were infected with HSV-1 using the mouse ocular model of HSV latency and reactivation. The current results indicate that p35 is an important determinant of viral replication in vivo.en_US
dc.publisherSpringer Verlagen_US
dc.rights© Journal of NeuroVirology, Inc. 2010en_US
dc.subjectcdk5en_US
dc.subjectHSV-1en_US
dc.subjectHSV-1 latency and reactivationen_US
dc.subjectp35en_US
dc.subjectp35 knockout miceen_US
dc.titleRole of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivoen_US
dc.typeArticleen_US
kusw.kuauthorHaenchen, Steve D.
kusw.kuauthorUtter, Jeff A.
kusw.kuauthorDobrowsky, Rick T.
kusw.kuauthorDavido, David J.
kusw.kudepartmentMolecular Biosciencesen_US
dc.identifier.doi10.3109/13550284.2010.513030en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC2975483en_US
dc.rights.accessrightsopenAccess


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