RRM2B Suppresses Activation of the Oxidative Stress Pathway and is Up-regulated by P53 During Senescence

• DOI: 10.1038/srep00822
• Publication Date: 2012-11-08T10:36:03Z
• Authors: Mei-Ling Kuo; Alexander J. Sy; Lijun Xue; Martin Chi; Michelle T. -C. Lee; Terence Yen; Mei-Iok Chiang; Lufen Chang; Peiguo Chu; Yun Yen
• Keywords: Senescence; Ribonucleotide reductase

RRM2B is the DNA damage-inducible small subunit of ribonucleotide reductase, rate-limiting enzyme in de novo deoxyribonucleoside triphosphate synthesis. Although implicated repair and maintenance mitochondrial content, regulation function senescence have not been previously established. Here, we show that highly induced a p53-dependent manner during primary human fibroblast IMR90 cells expressed at higher levels senescent precancerous prostatic intraepithelial neoplasm lesions compared to adjacent normal prostate glands. Paradoxically, silencing expression leads an increase level reactive oxygen species, membrane depolarization premature p38MAPK- young fibroblasts. Consistently, induction accelerated Rrm2b deficient mouse embryo Our data demonstrate by stress signals prior onset prevents oxidative stress-induced senescence.