Article: article from journal or magazin.
Caspase-induced inactivation of the anti-apoptotic TRAF1 during Fas ligand-mediated apoptosis.
The activation of the transcription factor NF-kappaB often results in protection against apoptosis. In particular, pro-apoptotic tumor necrosis factor (TNF) signals are blocked by proteins that are induced by NF-kappaB such as TNFR-associated factor 1 (TRAF1). Here we show that TRAF1 is cleaved after Asp-163 when cells are induced to undergo apoptosis by Fas ligand (FasL). The C-terminal cleavage product blocks the induction of NF-kappaB by TNF and therefore functions as a dominant negative (DN) form of TRAF1. Our results suggest that the generation of DN-TRAF1 is part of a pro-apoptotic amplification system to assure rapid cell death.
Antigens, CD95/physiology, Apoptosis/drug effects, Apoptosis/physiology, Apoptosis Regulatory Proteins, Burkitt Lymphoma, Caspases/metabolism, Cell Line, Fas Ligand Protein, Fibrosarcoma, Humans, Kidney, Membrane Glycoproteins/pharmacology, Membrane Glycoproteins/physiology, NF-kappa B/metabolism, Peptide Fragments/pharmacology, Proteins/antagonists & inhibitors, Proteins/genetics, Receptors, Tumor Necrosis Factor/physiology, Recombinant Proteins/antagonists & inhibitors, Recombinant Proteins/metabolism, Signal Transduction, TNF Receptor-Associated Factor 1, TNF-Related Apoptosis-Inducing Ligand, Transfection, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha/pharmacology
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