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

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 hepatocyte...

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Bibliographic Details
Published in:FEBS letters 2002-08, Vol.526 (1), p.38-42
Main Authors: Meisse, Delphine, Van de Casteele, Mark, Beauloye, Christophe, Hainault, Isabelle, Kefas, Benjamin A, Rider, Mark H, Foufelle, Fabienne, Hue, Louis
Format: Article
Language:English
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Summary: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.
ISSN:0014-5793
1873-3468
DOI:10.1016/S0014-5793(02)03110-1