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Permanent link (DOI): https://doi.org/10.7939/R30S8T

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HSV-1 Remodels PI3-Kinase/AKT Signaling Open Access

Descriptions

Other title
Subject/Keyword
Herpes
AKT
Us3
PI3K
UL46
HSV-1
PDGF
VP11/12
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Quach, Kevin
Supervisor and department
Smiley, James R. (Medical Microbiology and Immunology)
Examining committee member and department
Irvin, Randy (Medical Microbiology and Immunology)
Evans, David (Medical Microbiology and Immunology)
Magor, Katherine (Biological Science)
Ingham, Robert (Medical Microbiology and Immunology)
Department
Department of Medical Microbiology and Immunology
Specialization
Virology
Date accepted
2013-01-08T12:19:17Z
Graduation date
2013-06
Degree
Master of Science
Degree level
Master's
Abstract
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 abundant tegument protein VP11/12 is required for this effect. Although VP11/12 is essential for AKT activation, deleting VP11/12 has no detectable effect on HSV-1 induced phosphorylation of the examined downstream target proteins. Rather, the protein kinase US3 is required for the phosphorylation of AKT targets and thus serves as an AKT mimic. Our data indicate that VP11/12 and US3 do not collaborate to provide redundant coverage of key AKT targets during infection. Interestingly, HSV-1 attenuates signals from activated AKT induced by external growth factors. Remarkably, neither VP11/12 nor US3 is required for this effect.
Language
English
DOI
doi:10.7939/R30S8T
Rights
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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File title: Introduction
File author: Kevin Quach
Page count: 149
File language: en-US
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