Journal
MITOCHONDRIAL RESEARCH IN TRANSLATIONAL MEDICINE
Volume 1201, Issue -, Pages 72-78Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2010.05612.x
Keywords
oxidative stress; manganese superoxide dismutase; p53
Funding
- NATIONAL CANCER INSTITUTE [R01CA139843] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA139843] Funding Source: Medline
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Mitochondria are important sites of myriad metabolic activities. The actions of mitochondria must be carefully synchronized with other processes in the cell to maintain cellular homeostasis. Interorganellar communication between mitochondria and the nucleus is key for coordination of these cellular functions. Numerous signaling proteins and transcription factors are affected by reactive oxygen species and aid interorganellar communication. p53 is an important tumor suppressing protein that regulates many cellular activities, such as cell cycle regulation, DNA repair, and programmed cell death. p53 carries out these functions through both transcription-dependent and transcription-independent routes at mitochondria and the nucleus. Manganese superoxide dismutase (MnSOD), a p53-regulated gene that is a vital antioxidant enzyme localized in the matrix of mitochondria, scavenges reactive oxygen species. Recent studies suggest that mitochondria can regulate p53 activity and that assaults on the cell that affect mitochondrial ROS production and mitochondrial function can influence p53 activity. Cross-talk between mitochondria and p53 is important in normal cellular functions, and a breakdown in communication among mitochondria, p53, and the nucleus may have serious consequences in disease development.
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