Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivo
Previous 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 l...
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Published in | Journal of neurovirology Vol. 16; no. 5; pp. 405 - 409 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Heidelberg
Journal of Neurovirology
01.10.2010
Springer |
Subjects | |
Online Access | Get full text |
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Summary: | Previous 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Steve D. Haenchen and Jeff A. Utter contributed equally to this work. |
ISSN: | 1355-0284 1538-2443 |
DOI: | 10.3109/13550284.2010.513030 |