摘要
Dear Editor,Reactive oxygen species(ROS)can serve as intracellular signals that promote cell proliferation and survival at sub-toxic levels,or function as toxic substances that cause cell death and senescence at high levels(Weinberg and Chandel,2009).p53 plays a key role in the control of cellular response to ROS by upregulating the expression of either antioxidant genes under low level of oxidative stresses or pro-oxidative and apoptotic genes under high level of stresses(Vigneron and Vousden,2010;Hafsi and Hainaut,2011).However,how p53 differentially regulates gene expression in response to different ROS level remains elusive.△133p53 is an N-terminal truncated form of p53(Bourdon et al.,2005)and functions to antagonize p53 apoptotic activity and to promote DNA double-strand break repair(Chen et al.,2009;Aoubala et al.,2011;Gong et al.,2015).In this study,we investigated the functional interaction between p53 and △133p53 in response to various levels of ROS.
