p53 coordinates with △133p53 isoform to promote cell survival under low-level oxidative stress

• 来源期刊: 分子细胞生物学报（英文版）
• 年，卷（期）: 2016,（1）
• 页码范围: 88-90
• 页数: 3页
• 语种: 中文
• DOI: 10.1093/jmcb/mjv069

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.A133p53 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.