TRAF1 is a TNF inducible regulator of NF-kappaB activation

FEBS Lett. 1999 Oct 29;460(2):246-50. doi: 10.1016/s0014-5793(99)01356-3.

Abstract

Tumor necrosis factor receptor (TNFR)-associated factor TRAF1 was first identified as a component of the TNFR2 signalling complex. Unlike the other members of the TRAF family, TRAF1 lacks the N-terminal ring finger motif and has a tissue specific expression. Here we demonstrate that expression of TRAF1 is induced by TNF and the protein kinase C (PKC) activator PMA, but not by interleukin-1 (IL-1). TNF-induced upregulation of TRAF1 could be prevented by pretreatment of the cells with the proteasome inhibitor MG-132, whereas the PKC inhibitor Ro31-8220 was without effect. Interestingly, overexpression of TRAF1 in HEK293T completely prevented NF-kappaB activation induced by TNF, IL-1, or overexpression of TRAF2 or TRAF6. These data suggest that inducible expression of TRAF1 may serve a negative regulatory function in NF-kappaB signalling pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Dose-Response Relationship, Drug
  • Gene Expression Regulation*
  • Genes, Reporter
  • HeLa Cells
  • Humans
  • Interleukin-1 / metabolism
  • Interleukin-6 / metabolism
  • Kinetics
  • NF-kappa B / metabolism*
  • Plasmids
  • Precipitin Tests
  • Proteins / metabolism
  • Proteins / physiology*
  • Signal Transduction
  • TNF Receptor-Associated Factor 1
  • TNF Receptor-Associated Factor 2
  • Tetradecanoylphorbol Acetate / metabolism
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-1
  • Interleukin-6
  • NF-kappa B
  • Proteins
  • TNF Receptor-Associated Factor 1
  • TNF Receptor-Associated Factor 2
  • Tumor Necrosis Factor-alpha
  • Tetradecanoylphorbol Acetate