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Molecular and Cellular Biology, September 2004, p. 7878-7890, Vol. 24, No. 18
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.18.7878-7890.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

A Cellular RNA-Binding Protein Enhances Internal Ribosomal Entry Site-Dependent Translation through an Interaction Downstream of the Hepatitis C Virus Polyprotein Initiation Codon

Jong Heon Kim, Ki Young Paek, Sang Hoon Ha, Sungchan Cho, Kobong Choi, Chon Saeng Kim, Sung Ho Ryu, and Sung Key Jang*

NRL, PBC, Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, Kyungbuk, South Korea

Received 23 April 2004/ Returned for modification 17 May 2004/ Accepted 17 June 2004

Translational initiation of hepatitis C virus (HCV) mRNA occurs by internal entry of ribosomes into an internal ribosomal entry site (IRES) at the 5' nontranslated region. A region encoding the N-terminal part of the HCV polyprotein has been shown to augment the translation of HCV mRNA. Here we show that a cellular protein, NS1-associated protein 1 (NSAP1), augments HCV mRNA translation through a specific interaction with an adenosine-rich protein-coding region within the HCV mRNA. The overexpression of NSAP1 specifically enhanced HCV IRES-dependent translation, and knockdown of NSAP1 by use of a small interfering RNA specifically inhibited the translation of HCV mRNA. An HCV replicon RNA capable of mimicking the HCV proliferation process in host cells was further used to confirm that NSAP1 enhances the translation of HCV mRNA. These results suggest the existence of a novel mechanism of translational enhancement that acts through the interaction of an RNA-binding protein with a protein coding sequence.

* Corresponding author. Mailing address: NRL, PBC, Division of Molecular and Life Sciences, Pohang University of Science and Technology, Hyoja-Dong San 31, Pohang, Kyungbuk 790-784, South Korea. Phone: 82-54-279-2298. Fax: 82-54-279-8009. E-mail: sungkey{at}postech.ac.kr.

Molecular and Cellular Biology, September 2004, p. 7878-7890, Vol. 24, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.18.7878-7890.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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