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http://purl.uniprot.org/citations/16943283http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16943283http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16943283http://www.w3.org/2000/01/rdf-schema#comment"Hepatitis C virus (HCV) has been the subject of intensive studies for nearly two decades. Nevertheless, some aspects of the virus life cycle are still a mystery. The HCV nonstructural protein 5A (NS5A) has been shown to be a modulator of cellular processes possibly required for the establishment of viral persistence. NS5A is heavily phosphorylated, and a switch between a basally phosphorylated form of NS5A (p56) and a hyperphosphorylated form of NS5A (p58) seems to play a pivotal role in regulating HCV replication. Using kinase inhibitors that specifically inhibit the formation of NS5A-p58 in cells, we identified the CKI kinase family as a target. NS5A-p58 increased upon overexpression of CKI-alpha, CKI-delta, and CKI-epsilon, whereas the RNA interference of only CKI-alpha reduced NS5A hyperphosphorylation. Rescue of inhibition of NS5A-p58 was achieved by CKI-alpha overexpression, and we demonstrated that the CKI-alpha isoform is targeted by NS5A hyperphosphorylation inhibitors in living cells. Finally, we showed that down-regulation of CKI-alpha attenuates HCV RNA replication."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.org/dc/terms/identifier"doi:10.1128/jvi.01465-06"xsd:string
http://purl.uniprot.org/citations/16943283http://purl.org/dc/terms/identifier"doi:10.1128/jvi.01465-06"xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"De Francesco R."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"De Francesco R."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Di Pietro C."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Di Pietro C."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Neddermann P."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Neddermann P."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Quintavalle M."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Quintavalle M."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Sambucini S."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/author"Sambucini S."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/name"J. Virol."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/name"J. Virol."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/pages"11305-11312"xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/pages"11305-11312"xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/title"The alpha isoform of protein kinase CKI is responsible for hepatitis C virus NS5A hyperphosphorylation."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/title"The alpha isoform of protein kinase CKI is responsible for hepatitis C virus NS5A hyperphosphorylation."xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/volume"80"xsd:string
http://purl.uniprot.org/citations/16943283http://purl.uniprot.org/core/volume"80"xsd:string