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Internal translation initiation stimulates expression of the ARF/core+1 open reading frame of HCV genotype 1b
dc.creator | Boumlic, A. | en |
dc.creator | Vassilaki, N. | en |
dc.creator | Dalagiorgou, G. | en |
dc.creator | Kochlios, E. | en |
dc.creator | Kakkanas, A. | en |
dc.creator | Georgopoulou, U. | en |
dc.creator | Markoulatos, P. | en |
dc.creator | Orfanoudakis, G. | en |
dc.creator | Mavromara, P. | en |
dc.date.accessioned | 2015-11-23T10:24:08Z | |
dc.date.available | 2015-11-23T10:24:08Z | |
dc.date.issued | 2011 | |
dc.identifier | 10.1016/j.virusres.2010.10.007 | |
dc.identifier.issn | 0168-1702 | |
dc.identifier.uri | http://hdl.handle.net/11615/26419 | |
dc.description.abstract | The hepatitis C virus possesses an alternative open reading frame overlapping the Core gene, whose products are referred to as Core+1 or alternative reading frame (ARF) or F protein(s). Extensive studies on genotype HCV-1 a demonstrated that ribosomal frameshifting supports the synthesis of core+1 protein, when ten consecutive As are present within core codons 9-11 whereas, in the absence of this motif, expression of the core+1 ORF is mediated mainly by internal translation initiation. However, in HCV-1b, no Core+1 isoforms produced by internal translation initiation have been described. Using constructs which contain the Core/Core+1(342-770) region from previously described HCV-1b clinical isolates from liver biopsies, we provide evidence for the synthesis of Core+1 proteins by internal translation initiation in transiently transfected mammalian cells using nuclear or cytoplasmic expression systems. Site directed mutagenesis analyses revealed that (a) the synthesis of Core+1 proteins is independent from the polyprotein expression, as we observed an increase of Core+1 protein expression from constructs lacking the polyprotein translation initiator, (b) the main Core+1 product is expressed from AUG(85), similarly to the Core+1/S protein of HCV-1 a, (c) synthesis of Core+1 isoforms is also mediated from GUG(58) or under certain conditions GUG(26) internal codons, albeit at lower efficiency. Finally, comparable to HCV-1 a Core+1 proteins, the HCV-1 b Core+1 products are negatively regulated by core expression and the proteaosomal pathway. The expression of Core+1 ORF from HCV-1b clinical isolates and the preservation of translation initiation mechanism that stimulates its expression encourage investigating the role of these proteins in HCV pathogenesis. (c) 2010 Published by Elsevier B.V. | en |
dc.source | Virus Research | en |
dc.source.uri | <Go to ISI>://WOS:000287010300029 | |
dc.subject | HCV | en |
dc.subject | Core+1 | en |
dc.subject | ARFP | en |
dc.subject | Translation | en |
dc.subject | Mutagenesis | en |
dc.subject | HEPATITIS-C-VIRUS | en |
dc.subject | F-PROTEIN | en |
dc.subject | CORE PROTEIN | en |
dc.subject | HEPATOCELLULAR-CARCINOMA | en |
dc.subject | RNA | en |
dc.subject | REGION | en |
dc.subject | SEQUENCE | en |
dc.subject | CELLS | en |
dc.subject | REPLICATION | en |
dc.subject | ACTIVATION | en |
dc.subject | Virology | en |
dc.title | Internal translation initiation stimulates expression of the ARF/core+1 open reading frame of HCV genotype 1b | en |
dc.type | journalArticle | en |
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