Sustained activation of AMP-activated protein kinase induces c-Jun N-terminal kinase activation and apoptosis in liver cells
Sustained activation of AMP-activated protein kinase induces c-Jun N-terminal kinase activation and apoptosis in liver cells
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DOI：
10.1016/s0014-5793(02)03110-1
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发表时间：
2002-08-28
期刊：
影响因子：
3.5
通讯作者：
Hue, L
中科院分区：
文献类型：
--
作者：
Meisse, D;Van de Casteele, M;Hue, L
本工作的目的是研究持续激活AMP激活的蛋白激酶（AMPK）对肝细胞存活的影响。通过将FTO 2B细胞与AICA-核苷一起孵育（AICA-核苷转化为ZMP（一种AMP类似物））或通过用组成型活性形式的AMPK腺病毒转染肝细胞来实现AMPK激活。AMPK激活延长触发细胞凋亡和激活c-Jun N-末端激酶（JNK）和caspase-3。用分别抑制AMPK、JNK和半胱天冬酶活化的碘杀结核菌素、双香豆素和z-VAD-fatrin进行的实验支持了肝细胞中AMPK活化延长通过涉及JNK和半胱天冬酶-3的活化途径诱导细胞凋亡的观点。(C)2002年欧洲生物化学学会联合会。由Elsevier Science B. V.出版，版权所有。
The aim of this work was to study the effect of a sustained activation of AMP-activated protein kinase (AMPK) on liver cell survival. AMPK activation was achieved by incubating FTO2B cells with AICA-riboside, which is transformed into ZMP, an AMP analogue, or by adenoviral transfection of hepatocytes with a constitutively active form of AMPK. Prolonged AMPK activation triggered apoptosis and activated c-Jun N-terminal kinase (JNK) and caspase-3. Experiments with iodotubercidin, dicoumarol and z-VAD-fmk, which inhibited AMPK, JNK and caspase activation, respectively, supported the notion that prolonged AMPK activation in liver cells induces apoptosis through an activation pathway that involves JNK and caspase-3. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.