5'AMP-activated protein kinase alpha deficiency enhances stress-induced apoptosis in BHK and PC12 cells.

Détails

Ressource 1Demande d'une copie Sous embargo indéterminé.
Accès restreint UNIL
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_CBB2EB681B2D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
5'AMP-activated protein kinase alpha deficiency enhances stress-induced apoptosis in BHK and PC12 cells.
Périodique
Journal of cellular and molecular medicine
Auteur⸱e⸱s
Shaw M.M., Gurr W.K., McCrimmon R.J., Schorderet D.F., Sherwin R.S.
ISSN
1582-1838
ISSN-L
1582-1838
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
11
Numéro
2
Pages
286-298
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
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.
Mots-clé
AMP-Activated Protein Kinases, Animals, Apoptosis/physiology, Cell Line, Cell Line, Transformed, Cell Transformation, Viral, Cricetinae, Enzyme Activation, Multienzyme Complexes/deficiency, Multienzyme Complexes/genetics, Oxidative Stress, PC12 Cells, Protein Serine-Threonine Kinases/deficiency, Protein Serine-Threonine Kinases/genetics, Rats
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 13:59
Dernière modification de la notice
09/08/2024 15:52
Données d'usage