Titre
5'AMP-activated protein kinase alpha deficiency enhances stress-induced apoptosis in BHK and PC12 cells.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Shaw, M.M.
Auteure/Auteur
Gurr, W.K.
Auteure/Auteur
McCrimmon, R.J.
Auteure/Auteur
Schorderet, D.F.
Auteure/Auteur
Sherwin, R.S.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1582-1838
Statut éditorial
Publié
Date de publication
2007
Volume
11
Numéro
2
Première page
286
Dernière page/numéro d’article
298
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
5'AMP-activated protein kinase (AMPK) activation occurs under a variety of stress conditions but the role of this enzyme in the promotion or inhibition of stress-induced cell death is unclear. To address this issue, we transformed two different cell lines with shRNA-expressing plasmids, targeting the alpha subunit of AMPK, and verified AMPKalpha downregulation. The cell lines were then stressed by exposure to medium without glucose (PC12 cells) or with the viral thymidine kinase-specific DNA replication inhibitors: acyclovir, penciclovir and ganciclovir (herpes simplex virus thymidine kinase-expressing Baby Hamster Kidney cells). In non-AMPK-downregulated cells, these stress treatments induced AMPK upregulation and phosphorylation, leaving open the question whether the association of AMPK activation with stress-induced cell death reflects a successful death-promoting or an ineffective death-inhibiting activity. In AMPKalpha-deficient cells (expressing AMPKalpha-specific shRNAs or treated with Compound C) exposure to low glucose medium or DNA replication inhibitors led to an enhancement of cell death, indicating that, under the conditions examined, the role of activated AMPK is not to promote, but to protect from or delay stress-induced cell death.
PID Serval
serval:BIB_CBB2EB681B2D
PMID
Open Access
Oui
Date de création
2008-01-28T11:59:18.340Z
Date de création dans IRIS
2025-05-21T02:02:03Z
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17488477_BIB_CBB2EB681B2D.pdf
Version du manuscrit
published
Taille
981.16 KB
Format
Adobe PDF
PID Serval
serval:BIB_CBB2EB681B2D.P001
Somme de contrôle
(MD5):f05884c099c5d7ad6a7a9ee547c7a65c