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FEBS Lett. 2002 Aug 28;526(1-3):38-42.

Sustained activation of AMP-activated protein kinase induces c-Jun N-terminal kinase activation and apoptosis in liver cells.

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  • 1Hormone and Metabolic Research Unit, University of Louvain Medical School and Christian de Duve International Institute of Molecular and Cellular Pathology, Brussels, Belgium. delphine.meisse@horm.ucl.ac.be

Abstract

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.

PMID:
12208500
[PubMed - indexed for MEDLINE]
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