Upadhyay Sunil, Chatterjee Aditi, Trink Barry, Sommer Matthias, Ratovitski Edward, Sidransky David
Department of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Research Division, The Johns Hopkins University School of Medicine, 1550 Orleans Street, 5N.03 Baltimore, MD 21231, USA.
Biochem Biophys Res Commun. 2007 May 18;356(4):823-8. doi: 10.1016/j.bbrc.2007.01.168. Epub 2007 Feb 7.
We showed that TAp63gamma regulates hOGG1. Using chromatin immunoprecipitation (ChIP), we found that TAp63gamma binds to the hOGG1 promoter. Reintroduction of wild-type TAp63gamma into HEK 293 cells, induced transcription of hOGG1 promoter, leading to increase in RNA and protein. Using RNAi studies, we observed that TAp63gamma-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 TAp63gamma, suggesting a role for TAp63gamma in oxidative damage and repair.
我们发现TAp63γ可调节hOGG1。通过染色质免疫沉淀法（ChIP），我们发现TAp63γ与hOGG1启动子结合。将野生型TAp63γ重新导入HEK 293细胞，可诱导hOGG1启动子的转录，导致RNA和蛋白质水平增加。通过RNA干扰研究，我们观察到TAp63γ-RNA干扰导致HeLa细胞中hOGG1 RNA和蛋白质减少。hOGG1表达的这种降低与氧化损伤后细胞活力降低有关。综上所述，我们的结果表明hOGG1是TAp63γ的直接靶点，提示TAp63γ在氧化损伤和修复中发挥作用。
