JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dosch, T.
Right arrow Articles by Stauber, R. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dosch, T.
Right arrow Articles by Stauber, R. H.

 Previous Article  |  Next Article 

Journal of Virology, June 2001, p. 5677-5683, Vol. 75, No. 12
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.12.5677-5683.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

The Adenovirus Type 5 E1B-55K Oncoprotein Actively Shuttles in Virus-Infected Cells, Whereas Transport of E4orf6 Is Mediated by a CRM1-Independent Mechanism

Tanja Dosch,1 Florian Horn,1 Grit Schneider,1 Friedrich Krätzer,1 Thomas Dobner,2 Joachim Hauber,1 and Roland H. Stauber1,*

Institute for Clinical and Molecular Virology, University of Erlangen-Nürnberg, D-91054 Erlangen,1 and Institut für Medizinische Mikrobiologie und Hygiene, Universität Regensburg, D-93053 Regensburg,2 Germany

Received 16 January 2001/Accepted 20 March 2001

The E1B-55K and E4orf6 proteins of adenovirus type 5 are involved in viral mRNA export. Here we demonstrate that adenovirus infection does not inhibit the function of the E1B-55K nuclear export signal and that E1B-55K also shuttles in infected cells. Even during virus infection, E1B-55K was exported by the leptomycin B-sensitive CRM1 pathway, whereas E4orf6 transport appeared to be mediated by an alternative mechanism. Our results strengthen the potential role of E1B-55K as the "driving force" for adenoviral late mRNA export.

* Corresponding author. Mailing address: Institute for Clinical and Molecular Virology, University of Erlangen-Nürnberg, Schlossgarten 4, D-91054 Erlangen, Germany. Phone: (49)-9131-8522102. Fax: (49)-9131-8522101. E-mail: rdstaube{at}viro.med.uni-erlangen.de.

Journal of Virology, June 2001, p. 5677-5683, Vol. 75, No. 12
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.12.5677-5683.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2001 by the American Society for Microbiology. All rights reserved.