Fas ligand-induced c-Jun kinase activation in lymphoid cells requires extensive receptor aggregation but is independent of DAXX, and Fas-mediated cell death does not involve DAXX, RIP, or RAIDD

Détails

ID Serval
serval:BIB_9E45021E2C74
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Fas ligand-induced c-Jun kinase activation in lymphoid cells requires extensive receptor aggregation but is independent of DAXX, and Fas-mediated cell death does not involve DAXX, RIP, or RAIDD
Périodique
Journal of Immunology
Auteur⸱e⸱s
Villunger  A., Huang  D. C., Holler  N., Tschopp  J., Strasser  A.
ISSN
0022-1767 (Print)
Statut éditorial
Publié
Date de publication
08/2000
Volume
165
Numéro
3
Pages
1337-43
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Aug 1
Résumé
Jun kinase signaling can be elicited by death receptor activation, but the mechanism and significance of this event are still unclear. It has been reported that cross-linking Abs to Fas trigger c-Jun N-terminal kinase (JNK) signaling via caspase-mediated activation of MEKK1 (JNK kinase kinase), elevation of ceramide levels or by recruitment of death domain associated protein (DAXX) to Fas. The effect of physiological ligand for Fas on JNK signaling was never investigated, although evidence is accumulating that Fas ligand is able to induce cellular responses distinct from those evoked by Ab-mediated cross-linking of Fas. Therefore, we investigated the effect of Fas ligand on JNK signaling. Like its ability to induce cell death, Fas ligand reliably activated JNK only upon extensive aggregation of the receptor. Although this was partially dependent on caspase activation, DAXX was not required. DAXX and other death receptor-associated proteins, which have been reported to bind directly or indirectly to Fas, such as receptor interacting protein (RIP) and RIP-associated ICH-1/CED-3-homologous protein with a death domain (RAIDD), were shown to be dispensable for Fas ligand-induced apoptosis.
Mots-clé
Adaptor Proteins, Signal Transducing Animals Antigens, CD95/immunology/metabolism/*physiology Apoptosis/genetics/*immunology Carrier Proteins/biosynthesis/genetics/*physiology Caspases/physiology Cell Line, Transformed Enzyme Activation/immunology Fas Ligand Protein Genetic Vectors/chemical synthesis/pharmacology Humans *Intracellular Signaling Peptides and Proteins JNK Mitogen-Activated Protein Kinases Jurkat Cells Ligands Lymphocytes/cytology/*enzymology/immunology/metabolism Membrane Glycoproteins/immunology/metabolism/*physiology Mice Mitogen-Activated Protein Kinases/*metabolism *Nuclear Proteins Protein Biosynthesis Proteins/genetics/*physiology Receptor Aggregation/*immunology Receptor-Interacting Protein Serine-Threonine Kinases Signal Transduction/genetics/immunology Tumor Cells, Cultured
Pubmed
Web of science
Création de la notice
24/01/2008 16:18
Dernière modification de la notice
20/08/2019 16:04
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