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Spring 2011
VP16 initiates the HSV replication cycle by activating immediate early (IE) gene expression. It recruits the RNA pol II through an acidic C-terminal domain. The defective VP16 encoded by the V422 mutant of HSV-1 possesses a truncated C-terminal domain. Therefore, V422 replication is suppressed in...
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Characterization of the Herpes Simplex Virus 1 VP11/12-tyrosine based binding motifs for Src family kinases, p85, Grb2 and Shc
DownloadSpring 2018
Infection with HSV-1 triggers several events specifically designed to manipulate cell signal transduction pathways. Two major signaling cascades targeted by the virus are the PI3K/Akt-pathway and the TCR-signaling pathway. Prior to the studies presented in this thesis, it was known that the...
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Spring 2013
AKT inhibits apoptosis and stimulates cap-dependent translation by phosphorylating key downstream cellular proteins. Many viruses therefore activate the PI3-kinase-AKT signaling pathway to promote cell survival and viral protein synthesis. HSV-1 activates AKT during lytic infection and the...
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Fall 2013
Deregulated TNF signaling with elevated or decreased levels of TNF-induced apoptosis causes numerous inflammatory and cancerous diseases. Thus, there is a clear need to identify cellular proteins that regulate cell fate in the presence of TNF. RNA interference technology provides an excellent...
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Fall 2014
Infection with herpes simplex virus type 1 (HSV-1) leads to the rapid and complete loss of mitochondrial DNA (mtDNA) and mitochondrial messenger RNA (mt-mRNA), effectively eliminating gene expression within mitochondria. Previous work determined that a unique 3’ co-terminal transcript arising...
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Spring 2010
Infection of most cell types with herpes simplex virus (HSV) mutants lacking the activation functions of VP16 and/or ICP0 results in repression of viral gene expression. However, the human osteosarcoma cell line U2OS supports the replication of VP16 and ICP0 mutants to nearly wild type levels. ...