A Cellular RNA-Binding Protein Enhances Internal Ribosomal Entry Site-Dependent Translation through an Interaction Downstream of the Hepatitis C Virus Polyprotein Initiation Codon
Eukaryotic translation
NS2-3 protease
Coding region
Eukaryotic initiation factor
Eukaryotic Ribosome
DOI:
10.1128/mcb.24.18.7878-7890.2004
Publication Date:
2004-08-31T00:08:05Z
AUTHORS (8)
ABSTRACT
Translational initiation of hepatitis C virus (HCV) mRNA occurs by internal entry ribosomes into an ribosomal site (IRES) at the 5′ nontranslated region. A region encoding N-terminal part HCV polyprotein has been shown to augment translation mRNA. Here we show that a cellular protein, NS1-associated protein 1 (NSAP1), augments through specific interaction with adenosine-rich protein-coding within The overexpression NSAP1 specifically enhanced IRES-dependent translation, and knockdown use small interfering RNA inhibited An replicon capable mimicking proliferation process in host cells was further used confirm enhances These results suggest existence novel mechanism translational enhancement acts RNA-binding coding sequence.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (30)
CITATIONS (80)
EXTERNAL LINKS
PlumX Metrics
RECOMMENDATIONS
FAIR ASSESSMENT
Coming soon ....
JUPYTER LAB
Coming soon ....