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The cytokine-inducible zinc finger protein A20 inhibits IL-1-induced NF-kappaB activation at the level of TRAF6.

The zinc finger protein A20 is encoded by an immediate early response gene whose expression is induced by different inflammatory stimuli, including interleukin-1 (IL-1). Gene induction by IL-1 is mediated by activation of the transcription factor NF-kappaB, and requires the signal adapter protein TRAF6. The latter interacts with the NF-kappaB-inducing kinase NIK, which is believed to be part of the IkappaB kinase complex. Expression of A20 potently inhibits IL-1-induced NF-kappaB activation by an unknown mechanism. Inhibition of IL-1-induced NF-kappaB activation was found to be mediated by the C-terminal zinc finger-containing domain of A20. More importantly, we present evidence that A20 interferes with IL-1-induced NF-kappaB activation at the level of TRAF6, upstream of NIK. Moreover, A20 was shown to directly interact with TRAF6.

Pubmed ID: 9928991

Authors

  • Heyninck K
  • Beyaert R

Journal

FEBS letters

Publication Data

January 15, 1999

Associated Grants

None

Mesh Terms

  • Blotting, Western
  • Cell Line
  • DNA-Binding Proteins
  • Gene Expression Regulation
  • Humans
  • Interleukin-1
  • Intracellular Signaling Peptides and Proteins
  • Kidney
  • NF-kappa B
  • Nuclear Proteins
  • Precipitin Tests
  • Protein-Serine-Threonine Kinases
  • Proteins
  • Sequence Deletion
  • Signal Transduction
  • TNF Receptor-Associated Factor 1
  • TNF Receptor-Associated Factor 2
  • TNF Receptor-Associated Factor 6
  • Transcriptional Activation
  • Transfection
  • Tumor Necrosis Factor-alpha
  • Zinc Fingers