The peptidyl-prolyl isomerase Pin1 facilitates ...
Document type :
Article dans une revue scientifique: Article original
DOI :
PMID :
Permalink :
Title :
The peptidyl-prolyl isomerase Pin1 facilitates cytokine-induced survival of eosinophils by suppressing Bax activation.
Author(s) :
Shen, Zhong-Jian [Auteur]
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Schinzel, Anna [Auteur]
Borner, Christoph [Auteur]
University of Freiburg [Freiburg]
Malter, James S [Auteur]
University of Wisconsin School of Medicine and Public Health
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Schinzel, Anna [Auteur]
Borner, Christoph [Auteur]
University of Freiburg [Freiburg]
Malter, James S [Auteur]
University of Wisconsin School of Medicine and Public Health
Journal title :
Nature Immunology
Abbreviated title :
Nat Immunol
Volume number :
10
Pages :
257-265
Publisher :
Nature Publishing Group
Publication date :
2009-03-01
Article status :
Publié
ISSN :
1529-2916
English keyword(s) :
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
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
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [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 ...
Show more >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.Show less >
Show more >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.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Submission date :
2023-11-14T10:58:51Z
2024-05-23T13:10:56Z
2024-05-23T13:10:56Z
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