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Akt 依赖的转化:生长所涉及的远不止仅仅存活。

Akt-dependent transformation: there is more to growth than just surviving.

作者信息

Plas David R, Thompson Craig B

机构信息

Department of Genome Science, The Genome Research Institute, University of Cincinnati, OH 45237, USA.

出版信息

Oncogene. 2005 Nov 14;24(50):7435-42. doi: 10.1038/sj.onc.1209097.

DOI:10.1038/sj.onc.1209097
PMID:16288290
Abstract

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.

摘要

Akt/PKB蛋白激酶家族的激活会引发细胞大小、代谢和存活的增加。Akt通过肿瘤抑制因子的磷酸化依赖性失活和营养信号的激活来协调调节这些基本的细胞过程。Akt信号传导刺激葡萄糖和氨基酸的转运与代谢,进而支持mTOR依赖性的蛋白质翻译增加。此外,Akt激活引导细胞进行从氧化磷酸化到有氧糖酵解的代谢转换。虽然这种转换促进细胞生长,但它也使细胞存活依赖于细胞外营养物质的持续供应,而这些营养物质本身是Akt信号转导中必需的调节元件。

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