TWEAK can induce cell death via endogenous TNF and TNF receptor 1.

Détails

Ressource 1Télécharger: BIB_C46EED5E330C.P001.pdf (185.79 [Ko])
Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_C46EED5E330C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
TWEAK can induce cell death via endogenous TNF and TNF receptor 1.
Périodique
European Journal of Immunology
Auteur(s)
Schneider P., Schwenzer R., Haas E., Mühlenbeck F., Schubert G., Scheurich P., Tschopp J., Wajant H.
ISSN
0014-2980 (Print)
ISSN-L
0014-2980
Statut éditorial
Publié
Date de publication
1999
Volume
29
Numéro
6
Pages
1785-1792
Langue
anglais
Résumé
TWEAK is a recently cloned novel member of the TNF ligand family. Here we show that soluble TWEAK is sufficient to induce apoptosis in Kym-1 cells within 18 h. TWEAK-induced apoptosis is indirect and is mediated by the interaction of endogenous TNF and TNF receptor (TNFR)1, as each TNFR1-Fc, neutralizing TNF-specific antibodies and TNFR1-specific Fab fragments efficiently antagonize cell death induction. In addition to this indirect mode of action, co-stimulation of Kym-1 cells with TWEAK enhances TNFR1-mediated cell death induction. In contrast to TNF, TWEAK does only modestly activate NF-kappaB or c-jun N-terminal kinase (JNK) in Kym-1 cells. Although TWEAK binding to Kym-1 cells is easily detectable by flow cytometric analysis, we found neither evidence for expression of the recently identified TWEAK receptor Apo3/TRAMP/wsl/DR3/LARD, nor indications for direct interactions of TWEAK with TNFR. Together, these characteristics of TWEAK-induced signaling in Kym-1 cells argue for the existence of an additional, still undefined non-death domain-containing TWEAK receptor in Kym-1 cells.
Mots-clé
Antigens, CD/physiology, Apoptosis/drug effects, Apoptosis/physiology, Apoptosis Regulatory Proteins, Base Sequence, Carrier Proteins/genetics, Carrier Proteins/pharmacology, Cell Line, Humans, NF-kappa B/metabolism, Oligodeoxyribonucleotides/genetics, Oligodeoxyribonucleotides/metabolism, Receptors, Tumor Necrosis Factor/physiology, Receptors, Tumor Necrosis Factor, Member 25, Receptors, Tumor Necrosis Factor, Type I, Recombinant Proteins/genetics, Recombinant Proteins/pharmacology, Tumor Necrosis Factor-alpha/physiology, Tumor Necrosis Factors
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 16:19
Dernière modification de la notice
09/05/2019 0:56
Données d'usage