TRAIL Receptors 1 (DR4) and 2 (DR5) Signal FADD-Dependent Apoptosis and Activate NF-κB
Pascal Schneider,Margot Thome,Kim Burns,Jean-Luc Bodmer,Kay Hofmann,Takao Kataoka,Nils Holler,Jürg Tschopp +7 more
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TLDR
It is shown that TRAil-R1 can associate with TRAIL-R2, suggesting that TRAIL may signal through heteroreceptor signaling complexes, and can signal both death and gene transcription, functions reminiscent of those of TNFR1 and TRAMP.About:
This article is published in Immunity.The article was published on 1997-12-01 and is currently open access. It has received 702 citations till now. The article focuses on the topics: TRADD & FADD.read more
Citations
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Journal ArticleDOI
Activators and target genes of Rel/NF-kappaB transcription factors.
TL;DR: It is argued that NF-κB functions more generally as a central regulator of stress responses and pairing stress responsiveness and anti-apoptotic pathways through the use of a common transcription factor may result in increased cell survival following stress insults.
Journal ArticleDOI
Signalling pathways of the TNF superfamily: a double-edged sword.
TL;DR: Two different tumour-necrosis factors, first isolated in 1984, were found to be cytotoxic to tumour cells and to induce tumour regression in mice, and blockers of TNF have been approved for human use in treating TNF-linked autoimmune diseases.
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Targeted Disruption of the Mouse Caspase 8 Gene Ablates Cell Death Induction by the TNF Receptors, Fas/Apo1, and DR3 and Is Lethal Prenatally
Eugene Varfolomeev,Marcus Schuchmann,Victor Luria,N. Chiannilkulchai,Jacques S. Beckmann,Igor Mett,Denis V. Rebrikov,Vadim M Brodianski,Oliver Kemper,Orit Kollet,Tsvee Lapidot,Dror Soffer,Tama Sobe,Karen B. Avraham,Tanya Goncharov,Helmut Holtmann,Peter Lonai,David Wallach +17 more
TL;DR: Findings indicate that Caspase 8 plays a necessary and nonredundant role in death induction by several receptors of the TNF/NGF family and serves a vital role in embryonal development.
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Mature T lymphocyte apoptosis--immune regulation in a dynamic and unpredictable antigenic environment.
Michael J. Lenardo,K M Chan,Felicita Hornung,Hugh I. McFarland,Richard M. Siegel,Jin Wang,Lixin Zheng +6 more
TL;DR: Immunological, cellular, and molecular evidence indicates that throughout the life of a T cell, apoptosis may be evoked in excessive, harmful, or useless clonotypes to preserve a healthy and balanced immune system.
References
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Book
Molecular Cloning: A Laboratory Manual
TL;DR: Molecular Cloning has served as the foundation of technical expertise in labs worldwide for 30 years as mentioned in this paper and has been so popular, or so influential, that no other manual has been more widely used and influential.
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Apoptosis by death factor.
TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
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Identification and characterization of a new member of the TNF family that induces apoptosis
Steven R. Wiley,Ken Schooley,Pamela J. Smolak,Wenie S. Din,Chang-Pin Huang,Jillian Nicholl,Grant R. Sutherland,Terri Davis Smith,Charles Rauch,Craig A. Smith,Raymond G. Goodwin +10 more
TL;DR: A novel tumor necrosis factor (TNF) family member has been cloned and characterized, and the TRAIL gene is located on chromosome 3 at position 3q26, which is not close to any other known TNF ligand family members.
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Inhibition of death receptor signals by cellular FLIP
Martin Irmler,Margot Thome,Michael Hahne,Pascal Schneider,Kay Hofmann,Véronique Steiner,Jean-Luc Bodmer,Michael Schröter,Kim Burns,Chantal Mattmann,Donata Rimoldi,Lars E. French,Jürg Tschopp +12 more
TL;DR: The characterization of an inhibitor of apoptosis is reported, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues and may be implicated in tissue homeostasis as an important regulator of apoptotic regulation.
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FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis
TL;DR: Findings suggest that FADD may play an important role in the proximal signal transduction of Fas, a mutant of Fas possessing enhanced killing activity, but not the functionally inactive mutants Fas-LPR and Fas-FD8.