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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The coordinate regulation of the p53 and mTOR pathways in cells
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The coordinate regulation of the p53 and mTOR pathways in cells

机译：细胞中p53和mTOR途径的协调调控

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摘要

Cell growth and proliferation requires an intricate coordination between the stimulatory signals arising from nutrients and growth factors and the inhibitory signals arising from intracellular and extracellular stresses. Alteration of the coordination often causes cancer. In mammals, the mTOR (mammalian target of rapamycin) protein kinase is the central node in nutrient and growth factor signaling, and p53 plays a critical role in sensing genotoxic and other stresses. The results presented here demonstrate that activation of p53 inhibits mTOR activity and regulates its downstream targets, including autophagy, a tumor suppression process. Moreover, the mechanisms by which p53 regulates mTOR involves AMP kinase activation and requires the tuberous sclerosis (TSC) 1/TSC2 complex, both of which respond to energy deprivation in cells. In addition, glucose starvation not only signals to shut down mTOR, but also results in the transient phosphorylation of the p53 protein. Thus, p53 and mTOR signaling machineries can cross-talk and coordinately regulate cell growth, proliferation, and death.
机译：细胞的生长和增殖需要营养素和生长因子引起的刺激信号与细胞内和细胞外应激引起的抑制信号之间的复杂协调。协调性改变通常会导致癌症。在哺乳动物中，mTOR（雷帕霉素的哺乳动物靶标）蛋白激酶是营养和生长因子信号传导的中心节点，而p53在检测遗传毒性和其他压力中起关键作用。此处显示的结果证明p53的激活抑制mTOR活性并调节其下游靶标，包括自噬，肿瘤抑制过程。此外，p53调节mTOR的机制涉及AMP激酶激活，并需要结节性硬化症（TSC）1 / TSC2复合物，两者均对细胞中的能量缺乏作出反应。另外，葡萄糖饥饿不仅信号关闭mTOR，而且导致p53蛋白的瞬时磷酸化。因此，p53和mTOR信号传导机制可以相互干扰并协调调节细胞的生长，增殖和死亡。

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