The activation of the transcription factor NF-κB often results in protection against apoptosis. In particular, pro-apoptotic tumor necrosis factor (TNF) signals are blocked by proteins that are induced by NF-κB 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-κB 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. (C) 2000 Federation of European Biochemical Societies.
Irmler, M., Steiner, V., Ruegg, C., Wajant, H., & Tschopp, J. (2000). Caspase-induced inactivation of the anti-apoptotic TRAF1 during Fas ligand-mediated apoptosis. FEBS Letters, 468(2–3), 129–133. https://doi.org/10.1016/S0014-5793(00)01206-0