Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-2-7
pubmed:abstractText
In a previous study, we observed that hepatitis C virus (HCV) core protein specifically inhibits translation initiated by an HCV internal ribosome entry site (IRES). To investigate the mechanism by which down-regulation of HCV translation occurs, a series of mutations were introduced into the IRES element, as well as the core protein, and their effect on IRES activity examined in this study. We found that expression of the core protein inhibits HCV translation possibly by binding to a stem-loop IIId domain, particularly a GGG triplet within the hairpin loop structure of the domain, within the IRES. Basic-residue clusters located at the N-terminus of the core protein have an inhibitory effect on HCV translation, and at least one of three known clusters is required for inhibition. We propose a model in which competitive binding of the core protein for the IRES and 40S ribosomal subunit regulates HCV translation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
345
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
434-45
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Down-regulation of the internal ribosome entry site (IRES)-mediated translation of the hepatitis C virus: critical role of binding of the stem-loop IIId domain of IRES and the viral core protein.
pubmed:affiliation
Department of Virology II, National Institute of Infectious Diseases, Musashi-murayama, Tokyo 208-0011, Japan. shimoike@nih.go,jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't