Oh et al. showed that following UV radiation exposure, Wip1 is induced in a p53-dependent manner at later time points, and that Wip1 induction requires an intact NER system (59). The authors found that cells deficient in xeroderma pigmentosum complementation group B (XPB), a helicase that plays an essential role in NER (51), failed to induce Wip1 expression. Since NER is not functional in XPB cells, transcription-blocking UV radiation-induced DNA lesions persist at high levels. As the p53-dependent induction of large gene size targets, including Wip1, previously had been shown to be inhibited at high doses of UV radiation (60), the authors speculated that unrepaired lesions in the PPM1D gene in XPB cells prevented its transcription and expression (59). Therefore, NER is required for the repair of UV radiation-induced DNA lesions within the PPM1D gene and the subsequent p53-dependent induction at later time points after UV radiation exposure.
