Caspase-3 Protects Stressed Organs against Cell Death.

Détails

Ressource 1Télécharger: Mol. Cell. Biol.-2012-Khalil-4523-33 (1).pdf (4595.03 [Ko])
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_3A213E3293BE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Caspase-3 Protects Stressed Organs against Cell Death.
Périodique
Molecular and Cellular Biology
Auteur(s)
Khalil H., Peltzer N., Walicki J., Yang J.Y., Dubuis G., Gardiol N., Held W., Bigliardi P., Marsland B., Liaudet L., Widmann C.
ISSN
1098-5549 (Electronic)
ISSN-L
0270-7306
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
32
Numéro
22
Pages
4523-4533
Langue
anglais
Résumé
The ability to generate appropriate defense responses is crucial for the survival of an organism exposed to pathogenesis-inducing insults. However, the mechanisms that allow tissues and organs to cope with such stresses are poorly understood. Here we show that caspase-3-knockout mice or caspase inhibitor-treated mice were defective in activating the antiapoptotic Akt kinase in response to various chemical and environmental stresses causing sunburns, cardiomyopathy, or colitis. Defective Akt activation in caspase-3-knockout mice was accompanied by increased cell death and impaired survival in some cases. Mice homozygous for a mutation in RasGAP that prevents its cleavage by caspase-3 exhibited a similar defect in Akt activation, leading to increased apoptosis in stressed organs, marked deterioration of their physiological functions, and stronger disease development. Our results provide evidence for the relevance of caspase-3 as a stress intensity sensor that controls cell fate by either initiating a RasGAP cleavage-dependent cell resistance program or a cell suicide response.
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/11/2012 18:57
Dernière modification de la notice
08/05/2019 17:15
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