homeostatic regulation of p53 signaling mitochondrial energy metabolism to adapt to the movement of anti-aging.docVIP

 PAGE \* MERGEFORMAT 11 homeostatic regulation of p53 signaling mitochondrial energy metabolism to adapt to the movement of anti-aging On: May HU Yu Shao Xi Du Jifeng Liu Pengqi Chiu-Chao Ding Shuzhe [Keywords:] P53, mitochondria, SCO2, TIGAR, aging Solution is the key to cancer and aging and senescence in tumor occurrence and development mechanism of basic research breakthroughs in recent years on a wide range and depth of achievement. One of the most striking is the p53 (tumor suppressor) gene in the role of .2002 years, researchers in Texas that are not breed mice with the p53 gene, the results of these mice to form tumors at an early age. The researchers modified the p53 gene in another group of mice, resulting in p53 gene is too active, the results of this group of offspring of mice are not susceptible to cancer, but their life span shortened, without exception, (1). Obviously, to maintain the steady-state gene expression of p53 is to prevent cancer and premature aging of the strategy. cellular and molecular level studies have the p53 signal transduction theory of gradual fullness, and many related downstream signaling molecules upstream confirmed. tumor cells to increase oxygen consumption and aerobic glycolysis reduced so that the metabolic shift that is not economical and efficient way of energy supplied, This is the famous Valsalva effect. Matoba (2006 was first found on the cell culture, p53 (tumor suppressor balance of aerobic respiration and glycolysis is an extremely important material, p53 lead to loss of increased oxygen consumption and reduction of oxygen breathing and to facilitate steering glycolysis (2), p53 of this discovery has opened up a new vision, based on these findings, the topic will be the first in the overall level of adoption from animal experiments to explore the aging process, the movement to adapt to the p53 energy metabolism, physical exercise to explore the internal mechanism of aging. A signal loss of p53 tumor h