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. We found that DDB2 5'-UTR could initiate the downstream reporter, demonstrating that the 5'-UTR of DDB2 contained an IRES. The 5'-UTR of DDB2 was predicted into a relatively stable secondary structure by the Mfold program. We deleted the stem-loops in turn to analyze the core part of IRES and found that full length of the 5'-UTR was significant for the IRES activity. Furthermore, our data demonstrated that the DDB2 IRES activity was promoted during stress conditions. These results reveal a novel mechanism contributing to DDB2 expression.