Key result
A remarkably short 12-nucleotide internal ribosome entry site (IRES) lacking an AUG codon in the herpes simplex virus thymidine kinase gene permits low-level expression of active enzyme in a drug-resistant frameshift mutant.
Population
Herpes simplex virus mutant with a single-base deletion in the thymidine kinase gene and in vitro…
Design
Preclinical
Authors
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Suggests a mechanism for TK expression in drug-resistant HSV mutants; leaves open whether similar short IRES drive unrecognized polypeptides from eukaryotic mRNAs.
The discovery of a remarkably short IRES lacking an AUG codon in the viral tk gene suggests a mechanism for TK expression in drug-resistant mutants and implies many unrecognized polypeptides may be expressed at low levels from eukaryotic mRNAs.
Griffiths et al. (2005) studied Herpes simplex virus infection. C6-1C frameshift mutation in HSV tk gene vs. Wild-type tk gene was evaluated on Thymidine kinase (TK) activity and translation efficiency. A remarkably short 12-nucleotide internal ribosome entry site (IRES) lacking an AUG codon in the herpes simplex virus thymidine kinase gene permits low-level expression of active enzyme in a drug-resistant frameshift mutant.
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