蛋白激酶B
生物
PI3K/AKT/mTOR通路
细胞生物学
磷酸化
信号转导
原癌基因蛋白质c-akt
氧化磷酸化
激酶
细胞生长
生物化学
作者
David R. Plas,Craig B. Thompson
出处
期刊:Oncogene
[Springer Nature]
日期:2005-11-14
卷期号:24 (50): 7435-7442
被引量:426
标识
DOI:10.1038/sj.onc.1209097
摘要
Activation of the Akt/PKB protein kinase family triggers increases in cell size, metabolism and survival. Akt coordinately regulates these fundamental cellular processes through phosphorylation-dependent inactivation of tumor suppressors and activation of trophic signaling. Akt signaling stimulates transport and metabolism of both glucose and amino acids, which in turn support mTOR-dependent increases in protein translation. In addition, Akt activation directs cells to undertake a metabolic conversion from oxidative phosphorylation to aerobic glycolysis. Although this conversion promotes cell growth, it also renders cell survival dependent on a continuous supply of extracellular nutrients, which themselves are required regulatory elements in Akt signal transduction.
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