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A ubiquitin-specific protease possesses a decisive role for adenovirus replication and oncogene-mediated transformation.
PLoS Pathog. 9:e1003273 (2013)
Adenoviral replication depends on viral as well as cellular proteins. However, little is known about cellular proteins promoting adenoviral replication. In our screens to identify such proteins, we discovered a cellular component of the ubiquitin proteasome pathway interacting with the central regulator of adenoviral replication. Our binding assays mapped a specific interaction between the N-terminal domains of both viral E1B-55K and USP7, a deubiquitinating enzyme. RNA interference-mediated downregulation of USP7 severely reduced E1B-55K protein levels, but more importantly negatively affected adenoviral replication. We also succeeded in resynthesizing an inhibitor of USP7, which like the knockdown background reduced adenoviral replication. Further assays revealed that not only adenoviral growth, but also adenoviral oncogene-driven cellular transformation relies on the functions of USP7. Our data provide insights into an intricate mechanistic pathway usurped by an adenovirus to promote its replication and oncogenic functions, and at the same time open up possibilities for new antiviral strategies.
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8.136
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
E1b 55-kilodalton Protein ; Small-molecule Inhibitor ; Late Gene-expression ; Dna-replication ; Bioinformatics Analysis ; Tumor-suppressor ; Messenger-rna ; Wild-type ; P53 ; Degradation
Language
english
Publication Year
2013
HGF-reported in Year
2013
ISSN (print) / ISBN
1553-7366
e-ISSN
1553-7374
Journal
PLoS Pathogens
Quellenangaben
Volume: 9,
Issue: 3,
Article Number: e1003273
Publisher
Public Library of Science (PLoS)
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Immunology (IMI)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501793-001
PubMed ID
23555268
WOS ID
WOS:000316953800056
Scopus ID
84875991070
Erfassungsdatum
2013-05-03