The role of p53 in cell metabolism

The p53 tumor suppressor gene has recently been shown to mediate metabolic changes in cells under physiological and pathological conditions. It has been revealed that p53 regulates energy metabolism, oxidative stress, and amino acid metabolism through balancing glycotysis and oxidative phosphorylati...

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Published inActa pharmacologica Sinica Vol. 31; no. 9; pp. 1208 - 1212
Main Authors Zhang, Xing-ding, Qin, Zheng-hong, Wang, Jin
Format Journal Article
LanguageEnglish
Published United States Nature Publishing Group 01.09.2010
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Summary:The p53 tumor suppressor gene has recently been shown to mediate metabolic changes in cells under physiological and pathological conditions. It has been revealed that p53 regulates energy metabolism, oxidative stress, and amino acid metabolism through balancing glycotysis and oxidative phosphorylation (OXPHOS) as well as the autophagy pathway, p53 is activated by metabolic stress through AMP-activated protein kinase (AMPK) and the mammalian target of rapamycin (mTOR) signaling pathways, p53 regulates OXPHOS through the transcriptional regulation of fructose-2,6-bisphosophatase, TP53-induced glycolysis regulator (TIGAR) and synthesis of cytochrome c oxidase (SC02) subunit of complex iV of the electron transport chain, p53 also indirectly influences the energy metabolism through regulating glucose transporter (GLUT) expression, glutaminase 2 (GLS2) and fatty acid synthase (FAS). In addition, p53 regulates autophagy to provide cell metabolites for surviving through damage regulated autophagy modulator (DRAM1). Here we review the recent findings to elucidate the important role of p53 in cell metabolism.
Bibliography:Q2
damage-regulated autophagy modulator
tumor suppressor 53; glycolysis; oxidative phosphorylation; TP53-induced glycolysis regulator; damage-regulated autophagy modulator
glycolysis
Q251
TP53-induced glycolysis regulator
tumor suppressor 53
oxidative phosphorylation
31-1347/R
ObjectType-Article-2
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content type line 23
ObjectType-Review-1
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ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2010.151