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首页> 外文期刊>Cellular Signalling >The protein kinase B/Akt signalling pathway in human malignancy [Review]
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The protein kinase B/Akt signalling pathway in human malignancy [Review]

机译：蛋白激酶B / Akt信号通路在人类恶性肿瘤中的作用[综述]

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摘要

Protein kinase B or Akt (PKB.Akt) is a serine threonine kinase. which in mammals comprises three highly homologous members known as PKBalpha (Akt1). PKB3 (Akt2). Laid PKBgamma (Akt3). PKB Akt is activated in cells exposed to diverse stimuli such as hormones. growth factors, and extracellular Matrix components. The actuation mechanism remains to be fully characterised but occurs downstream of phosphoinositide 3-kinase (PI-3K). PI-3K generate, phosphatidylinositol-3,4,5-trisphosphate (PIP3), a lipid second messenger essential for the translocation of PKB.Akt to the plasma membrane where it is phosphorylated and activated by phosphoinositide-dependent kinase-l (PDK-1) and possibly other kinases. PKB.Akt phosphorylate and regulates the function of many cellular proteins in coked in processes that include metabolism, apoptosis, and proliferation. Recent evidence indicates that PKB Akt is frequently constitutively active in many types of human cancer. Constitutive PKB Akt activation can occur due to amplification of PKB.Akt genes or as a result of mutations in components of the signalling pathway that activates PKB.Akt. Although the mechanisms have not yet been Puny characterised, constitutive PKB.Akt signalling is believed to promote proliferation and increased cell survival and thereby contributing to cancer progression. This review surveys recent de developments in understanding the mechanisms and consequences of PKB.Akt activation in human malignancy. (C) 2002 Elsevier Science Ire. All rights reserved. [References: 196]
机译：蛋白激酶B或Akt（PKB.Akt）是丝氨酸苏氨酸激酶。它在哺乳动物中包含三个高度同源的成员，称为PKBalpha（Akt1）。 PKB3（Akt2）。放置的PKBgamma（Akt3）。 PKB Akt在暴露于多种刺激（例如激素）的细胞中被激活。生长因子和细胞外基质成分。致动机理尚待充分表征，但发生在磷酸肌醇3-激酶（PI-3K）的下游。 PI-3K产生磷脂酰肌醇-3,4,5-三磷酸酯（PIP3），这是PKB易位的脂质第二信使.Akt转移至质膜，并被磷酸肌醇依赖性激酶-1（PDK- 1）以及其他激酶。 PKB.Akt磷酸化并调节焦化过程中许多细胞蛋白的功能，包括代谢，凋亡和增殖。最近的证据表明，PKB Akt在许多类型的人类癌症中通常具有组成型活性。组成性PKB Akt激活可能是由于PKB.Akt基因的扩增或激活PKB.Akt的信号通路成分突变的结果。尽管尚未确定Puny的机制，但据信组成型PKB.Akt信号传导可促进增殖并提高细胞存活率，从而促进癌症进展。这篇综述调查了最近的发展，了解了人类恶性肿瘤中PKB.Akt激活的机制和后果。 （C）2002 Elsevier Science Ire。版权所有。 [参考：196]

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