文摘
We showed that TAp63γ regulates hOGG1. Using chromatin immunoprecipitation (ChIP), we found that TAp63γ binds to the hOGG1 promoter. Reintroduction of wild-type TAp63γ into HEK 293 cells, induced transcription of hOGG1 promoter, leading to increase in RNA and protein. Using RNAi studies, we observed that TAp63γ-RNAi resulted in reduced hOGG1 RNA and protein in HeLa cells. This decrease in hOGG1 expression was associated with reduced cell viability upon oxidative damage. Taken together, our results indicate that hOGG1 is a direct target of TAp63γ, suggesting a role for TAp63γ in oxidative damage and repair.