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Journal article

Caspase-induced inactivation of the anti-apoptotic TRAF1 during Fas ligand-mediated apoptosis.

  • 2000-02-29
Published in:
  • FEBS letters. - 2000
Apoptosis
Apoptosis Regulatory Proteins
Burkitt Lymphoma
Caspases
Cell Line
Fas Ligand Protein
Fibrosarcoma
Humans
Kidney
Membrane Glycoproteins
NF-kappa B
Peptide Fragments
Proteins
Receptors, Tumor Necrosis Factor
Recombinant Proteins
Signal Transduction
TNF Receptor-Associated Factor 1
TNF-Related Apoptosis-Inducing Ligand
Transfection
Tumor Cells, Cultured
Tumor Necrosis Factor-alpha
fas Receptor
English 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.
Language
  • English
Open access status
bronze
Identifiers
Persistent URL
https://sonar.ch/global/documents/277808
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