Journal
FEBS LETTERS
Volume 526, Issue 1-3, Pages 38-42Publisher
WILEY
DOI: 10.1016/S0014-5793(02)03110-1
Keywords
AICA-riboside; AMP-activated protein kinase; apoptosis; c-Jun; N-terminal kinase; hepatocyte
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available