Sarnowska Elżbieta, Balcerak Anna, Olszyna-Serementa Marta, Kotlarek Daria, Sarnowski Tomasz J, Siedlecki Janusz A
Zakład Onkologii Molekularnej i Translacyjnej, Centrum Onkologii Instytutu im. Marii Skłodowskiej - Curie, Warszawa.
Postepy Hig Med Dosw (Online). 2013 Aug 5;67:750-60. doi: 10.5604/17322693.1061403.
AMP-activated protein kinase (AMPK) is one of the major energy sensor at both: cellular and whole body level. It exists as heterotrimer containing three subunits: the catalytic α subunit, β and regulatory γ. AMPK is localized both in the cytoplasm and in the nucleus. It is activated by increasing concentrations of AMP during the energy shortage, causing activation of catabolic pathways and inhibition of energy consuming processes. AMPK activity can be regulated allosterically: by binding AMP to a regulatory γ subunit, as well as by phosphorylation on Thr172 of the catalytic α subunit by other kinases. Activated AMPK can effectively inhibit the mTOR pathway which is hyperactive in many types of cancer. On the other hand AMPK inactivation associates with the type II diabetes, diet-induced obesity, insulin resistance and the development of other metabolic disorders. The AMPK dysfunction is also observed in inflammation. It was discovered during last years that abnormalities in the AMPK function can induce the metabolic reprogramming in cancer cells known as the Warburg effect. Additionally, AMPK is activated during irradiation. Its activation leads to inhibition of growth. On the other hand, active AMPK enables cells to survive in difficult conditions such as hypoxia, or glucose deprivation. Because of its crucial role in maintaining of the energy homeostasis AMPK is an excellent therapeutic target. However, it still remains unknown what is better: to activate or inhibit the AMPK function.
AMP激活的蛋白激酶(AMPK)是细胞和全身水平上主要的能量传感器之一。它以包含三个亚基的异源三聚体形式存在:催化性α亚基、β亚基和调节性γ亚基。AMPK定位于细胞质和细胞核中。在能量短缺期间,它通过增加AMP浓度而被激活,从而导致分解代谢途径的激活和能量消耗过程的抑制。AMPK的活性可以通过变构调节:通过将AMP与调节性γ亚基结合,以及通过其他激酶对催化性α亚基的苏氨酸172进行磷酸化来调节。激活的AMPK可以有效抑制在许多类型癌症中过度活跃的mTOR途径。另一方面,AMPK失活与II型糖尿病、饮食诱导的肥胖、胰岛素抵抗以及其他代谢紊乱的发展有关。在炎症中也观察到AMPK功能障碍。在过去几年中发现,AMPK功能异常可诱导癌细胞中的代谢重编程,即瓦伯格效应。此外,AMPK在辐射期间被激活。其激活导致生长抑制。另一方面,活跃的AMPK使细胞能够在诸如缺氧或葡萄糖剥夺等困难条件下存活。由于其在维持能量稳态中的关键作用,AMPK是一个极好的治疗靶点。然而,激活还是抑制AMPK功能更好仍然未知。