Skip Navigation



Nucleic Acids Research Advance Access published online on November 14, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn901
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (6928K) Freely available
Right arrow Screen PDF (634K) Freely available
Right arrow Supplementary Data
Right arrowOA All Versions of this Article:
37/1/47    most recent
gkn901v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Lin, J.-Y.
Right arrow Articles by Shih, S.-R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, J.-Y.
Right arrow Articles by Shih, S.-R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Far upstream element binding protein 2 interacts with enterovirus 71 internal ribosomal entry site and negatively regulates viral translation

Jing-Yi Lin1,2,3, Mei-Ling Li1,5 and Shin-Ru Shih1,2,3,4,*

1Research Center for Emerging Viral Infections, 2Department of Medical Biotechnology and Laboratory Science, 3Graduate Program in Biomedical Science, Chang Gung University, Tao-Yuan, 4Division of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan and 5Department of Molecular Genetics, Microbiology and Immunology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ, USA

*To whom correspondence should be addressed. Tel: +886 3 2118800 (ext. 5497); Fax: +886 3 2118174; Email: srshih{at}mail.cgu.edu.tw

Received July 28, 2008. Revised October 25, 2008. Accepted October 27, 2008.

An internal ribosomal entry site (IRES) that directs the initiation of viral protein translation is a potential drug target for enterovirus 71 (EV71). Regulation of internal initiation requires the interaction of IRES trans-acting factors (ITAFs) with the internal ribosomal entry site. Biotinylated RNA-affinity chromatography and proteomic approaches were employed to identify far upstream element (FUSE) binding protein 2 (FBP2) as an ITAF for EV71. The interactions of FBP2 with EV71 IRES were confirmed by competition assay and by mapping the association sites in both viral IRES and FBP2 protein. During EV71 infection, FBP2 was enriched in cytoplasm where viral replication occurs, whereas FBP2 was localized in the nucleus in mock-infected cells. The synthesis of viral proteins increased in FBP2-knockdown cells that were infected by EV71. IRES activity in FBP2-knockdown cells exceeded that in the negative control (NC) siRNA-treated cells. On the other hand, IRES activity decreased when FBP2 was over-expressed in the cells. Results of this study suggest that FBP2 is a novel ITAF that interacts with EV71 IRES and negatively regulates viral translation.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Antimicrob. Agents Chemother.Home page
T.-C. Chen, H.-Y. Chang, P.-F. Lin, J.-H. Chern, J. T.-A. Hsu, C.-Y. Chang, and S.-R. Shih
Novel Antiviral Agent DTriP-22 Targets RNA-Dependent RNA Polymerase of Enterovirus 71
Antimicrob. Agents Chemother., July 1, 2009; 53(7): 2740 - 2747.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.