Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10871995 | FEBS Letters | 2009 | 5 Pages |
Abstract
Many viral mRNAs contain a 5â²-UTR RNA element called internal ribosome-entry site (IRES), which bypasses the requirement of some canonical initiation factors allowing cap-independent translation. The IRES of hepatitis-C virus drives translation by directly recruiting 40S ribosomal subunits and binds to eIF3 which plays a critical role in both cap-dependent and cap-independent translation. However, the molecular basis for eIF3 activity in either case remains enigmatic. Here we report that subunit b of the eIF3 complex directly binds to HCV IRES domain III via its N-terminal-RRM. Because eIF3b was previously shown to be involved in eIF3j binding, biological implications are discussed.
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Authors
Julien Pérard, Rodolfo Rasia, Jan Medenbach, Isabel Ayala, Jérôme Boisbouvier, Emmanuel Drouet, Florence Baudin,