[No authors listed]
The Fos protoâoncogene, activator proteinâ1 (APâ1) transcription factor subunit (câfos) gene, a member of the immediate early gene family, encodes câFos, which is a subunit of the APâ1 transcription factor. The present study aimed to investigate the mechanism by which the translation efficiency of câfos mRNA is upregulated when cellular protein synthesis is shut off. The result of western blotting revealed that the protein expression levels of câFos were increased in rhabdomyosarcoma cells infected with enterovirus 71 (EV71) compared with uninfected cells. PCR was used to get the câfos 5'âuntranslated region (UTR). The luciferase assay of a bicistronic vector containing the câfos 5'UTR revealed that the câfos 5'UTR contains an internal ribosome entry site (IRES) sequence and a 175 nucleotide sequence (between 31 and 205 nt) that is essential for IRES activity. Analysis of potential IRES transâacting factors revealed that poly(C)âbinding protein 2 (PCBP2) negatively regulated the activity of the câfos IRES, whereas the La autoantigen (La) positively regulated its activity. The results of RNAâprotein immunoprecipitation demonstrated that both PCBP2 and La bound to the câfos 5'UTR. Furthermore, the IRES activity of in vitroâtranscribed câfos mRNA was upregulated during EV71 infection. The present study suggested a mechanism for the effect of viral infection on host genes, and provided a novel target for gene translation regulation.
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