Key result
Mutation analysis of the PSIV-IRES element identified two new pseudoknots and confirmed a tertiary structure model for methionine-independent translation initiation applicable to CrPV-like viruses.
Population
Plautia stali intestine virus internal ribosome entry site element and other cricket paralysis-like viruses
Comparison
Compensatory mutations introduced into the… vs Wild-type/unmutated PSIV IRES element
Design
Preclinical
Authors
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Refines IRES structure model in CrPV-like viruses; hypothesis-generating for antivirals with no immediate clinical relevance.
The study establishes a tertiary structure model of the PSIV-IRES element, demonstrating that multiple pseudoknots are essential for methionine-independent translation initiation in CrPV-like viruses.
Kanamori et al. (2001) studied this question. Site-directed mutagenesis of PSIV-IRES vs. Wild-type PSIV-IRES was evaluated on IRES-mediated translation activity (capsid protein production in vitro). Mutation analysis of the PSIV-IRES element identified two new pseudoknots and confirmed a tertiary structure model for methionine-independent translation initiation applicable to CrPV-like viruses.
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