Abstract
In herpes simplex virus, lytic replication is initiated by the viral transactivator VP16 acting with cellular cofactors Oct-1 and HCF-1. Although this activator complex has been studied in detail, the role of HCF-1 remains elusive. Here, we show that HCF-1 contains an activation domain (HCF-1(AD)) required for maximal transactivation by VP16 and its cellular counterpart LZIP. Expression of the VP16 cofactor p300 augments HCF-1(AD) activity, suggesting a mechanism of synergy. Infection of cells lacking the HCF-1(AD) leads to reduced viral immediate-early gene expression and lowered viral titers. These findings underscore the importance of HCF-1 to herpes simplex virus replication and VP16 transactivation.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Base Sequence
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Cell Line
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Cyclic AMP Response Element-Binding Protein
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HeLa Cells
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Herpes Simplex Virus Protein Vmw65 / metabolism*
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Host Cell Factor C1
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Humans
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In Vitro Techniques
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Leucine Zippers
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Models, Biological
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Molecular Sequence Data
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Plasmids / genetics
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Protein Structure, Tertiary
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Protein Subunits
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Proteins / chemistry*
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Proteins / genetics
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Proteins / metabolism
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Simplexvirus / genetics*
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Simplexvirus / physiology*
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Transcription Factors / metabolism*
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Transcriptional Activation
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Virus Replication
Substances
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CREB3 protein, human
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Cyclic AMP Response Element-Binding Protein
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HCFC1 protein, human
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Herpes Simplex Virus Protein Vmw65
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Host Cell Factor C1
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Protein Subunits
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Proteins
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Transcription Factors