ÃÂ133p53 Functions to Maintain Redox Homeostasis in Response to Low ROS Stresses
Kunpeng Jiang, Jun Chen*
Key Laboratory for Molecular Animal Nutrition, Ministry of Education, College of Life Sciences, Zhejiang University, Hangzhou, PR China
- *Corresponding Author:
- Jun Chen
Key Laboratory for Molecular Animal Nutrition
Ministry of Education, College of Life Sciences
Zhejiang University, 866 Yu Hang Tang Road
Hangzhou, 310058, PR China
E-mail: [email protected]
Received date: December 16, 2016; Accepted date: December 29, 2016; Published date: December 31, 2016
Citation: Jiang K, Chen J (2016) Δ133p53 Functions to Maintain Redox Homeostasis in Response to Low ROS Stresses. Single Cell Biol 5:154. doi: 10.4172/2168-9431.1000154
Copyright: © 2016 Jiang K, et al. This is an open-access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Reactive oxygen species (ROS) can serve as intracellular signals that promote cell proliferation and survival, or as toxicants that cause abnormal cell death and senescence. Tumour repressor p53 is a ROS-active transcription factor that upregulates the expression of antioxidant genes during low oxidative stresses, but promotes the expression of pro-oxidative and apoptotic genes during high level stresses. The underlying mechanisms for p53 selectively to transcribe different groups of genes remain elusive. We recently found that p53 isoform Δ133p53 is strongly induced by a low concentration of H2O2 (50 μM), as opposed to higher concentrations, and functions to promote cell survival. Under the low oxidative stress, Δ133p53 is required for p53 to selectively upregulate the transcription of the antioxidant genes SESN1 and SOD1 by binding to their promoters. The knockdown of either p53 or Δ133p53 in low oxidative stresses increases the intracellular O2•– level, which results in accumulation of DNA damage, cell growth arrest at the G2 phase that in turn leads to enhanced cell senescence. Our findings suggest that an induction of Δ133p53 may correlate with ageing and human pathologies associated with oxidative stresses.