Gong Lu, Chen Jun
Key laboratory for Molecular Animal Nutrition, Ministry of Education, College of Life Sciences, Zhejiang University , Hangzhou, China.
Mol Cell Oncol. 2015 May 27;3(1):e1033587. doi: 10.1080/23723556.2015.1033587. eCollection 2016 Jan.
In response to DNA damage, p53 (TP53, best known as p53) is quickly activated leading to cell cycle arrest or apoptosis to ensure genomic integrity; however, this represses DNA double-strand break (DSB) repair. Our recent work revealed that Δ113p53/Δ133p53 protein is accumulated at a later stage upon DNA DSB stress to switch p53 signaling from repression to promotion of DNA DSB repair.
响应DNA损伤时,p53(TP53,最为人所知的名称是p53)会迅速被激活,导致细胞周期停滞或凋亡,以确保基因组完整性;然而,这会抑制DNA双链断裂(DSB)修复。我们最近的研究表明,在DNA DSB应激后期,Δ113p53/Δ133p53蛋白会积累,从而将p53信号从抑制DNA DSB修复转变为促进DNA DSB修复。