The 5'-UTR of DDB2 harbors an IRES element and upregulates translation during stress conditions.

DDB2 is a tumor-inhibiting factor not only involved a major DNA repair mechanism in the Nucleotide Excision Repair (NER), but also correlated with cell apoptosis in the DNA damage response pathway. During serum-starvation, we noted that the translation levels of DDB2 were increased. To evaluate whether the 5'-UTR of DDB2 harbors an IRES element, we used a bicistronic luciferase plasmid with the 5'-UTR of DDB2 inserted between two cistron coding regions.