Titre :

The peptidyl-prolyl isomerase Pin1 facilitates cytokine-induced survival of eosinophils by suppressing Bax activation.

Auteur(s) :

Shen, Zhong-Jian [Auteur]
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Schinzel, Anna [Auteur]
Borner, Christoph [Auteur]

Malter, James S [Auteur]
University of Wisconsin School of Medicine and Public Health

Titre de la revue :

Nature Immunology

Nom court de la revue :

Nat Immunol

Numéro :

10

Pagination :

257-265

Éditeur :

Nature Publishing Group

Date de publication :

2009-03-01

Statut de l’article :

Publié

ISSN :

1529-2916

Mot(s)-clé(s) en anglais :

Cell Death
Cell Survival
Cells, Cultured
Eosinophils
Extracellular Signal-Regulated MAP Kinases
Granulocyte-Macrophage Colony-Stimulating Factor
Humans
Interleukin-5
Mitochondria
NIMA-Interacting Peptidylprolyl Isomerase
Peptidylprolyl Isomerase
Phosphorylation
Protein Transport
bcl-2-Associated X Protein

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

The mechanisms by which cytokine signals prevent the activation and mitochondrial targeting of the proapoptotic protein Bax are unclear. Here we show, using primary human eosinophils, that in the absence of the prosurvival ...
Lire la suite >The mechanisms by which cytokine signals prevent the activation and mitochondrial targeting of the proapoptotic protein Bax are unclear. Here we show, using primary human eosinophils, that in the absence of the prosurvival cytokines granulocyte-macrophage colony-stimulating factor and interleukin 5, Bax spontaneously underwent activation and initiated mitochondrial disruption. Inhibition of Bax resulted in less eosinophil apoptosis, even in the absence of cytokines. Granulocyte-macrophage colony-stimulating factor induced activation of the kinase Erk1/2, which phosphorylated Thr167 of Bax; this facilitated new interaction of Bax with the prolyl isomerase Pin1. Blockade of Pin1 led to cleavage and mitochondrial translocation of Bax and caspase activation, regardless of the presence of cytokines. Our findings indicate that Pin1 is a key mediator of prosurvival signaling and is a regulator of Bax function.Lire moins >

Langue :

Anglais

Comité de lecture :

Oui

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

Université de Lille
Inserm
CHU Lille

Collections :

• Autres travaux scientifiques

Date de dépôt :

2023-11-14T10:58:51Z
2024-05-23T13:10:56Z