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FADD/MORT1 and caspase-8 are recruited to TRAIL receptors 1 and 2 and are essential for apoptosis mediated by TRAIL receptor 2

Apoptosis induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL/APO-2L) has been shown to exert important functions during various immunological processes. The involvement of the death adaptor proteins FADD/MORT1, TRADD, and RIP and the apoptosis-initiating caspases-8 and -...

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Bibliographic Details
Main Authors: Sprick, Martin (Author) , Weigand, Markus A. (Author) , Krammer, Peter H. (Author) , Walczak, Henning (Author)
Format: Article (Journal)
Language:English
Published: 2000
In: Immunity
Year: 2000, Volume: 12, Issue: 6, Pages: 599-609
ISSN:1097-4180
DOI:10.1016/S1074-7613(00)80211-3
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/S1074-7613(00)80211-3
Verlag, lizenzpflichtig, Volltext: https://www.cell.com/immunity/abstract/S1074-7613(00)80211-3
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Author Notes:Martin R. Sprick, Markus A. Weigand, Eva Rieser, Charles T. Rauch, Peter Juo, John Blenis, Peter H. Krammer, and Henning Walczak
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Summary:Apoptosis induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL/APO-2L) has been shown to exert important functions during various immunological processes. The involvement of the death adaptor proteins FADD/MORT1, TRADD, and RIP and the apoptosis-initiating caspases-8 and -10 in death signaling by the two death-inducing TRAIL receptors 1 and 2 (TRAIL-R1 and TRAIL-R2) are controversial. Analysis of the native TRAIL death-inducing signaling complex (DISC) revealed ligand-dependent recruitment of FADD/MORT1 and caspase-8. Differential precipitation of ligand-stimulated TRAIL receptors demonstrated that FADD/MORT1 and caspase-8 were recruited to TRAIL-R1 and TRAIL-R2 independently of each other. FADD/MORT1- and caspase-8-deficient Jurkat cells expressing only TRAIL-R2 were resistant to TRAIL-induced apoptosis. Thus, FADD/MORT1 and caspase-8 are essential for apoptosis induction via TRAIL-R2.
Item Description:Elektronische Reproduktion der Druckausgabe
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Physical Description:Online Resource
ISSN:1097-4180
DOI:10.1016/S1074-7613(00)80211-3

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