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Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation

S Aizawa1, H Nakano, T Ishida

  • 1Department of Pathology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108, Japan.

The Journal of Biological Chemistry
|January 24, 1997
PubMed

Insights

CD30 signaling activates nuclear factor kappaB (NFkappaB) through interactions with TRAF2 and TRAF5. These tumor necrosis factor receptor-associated factor proteins bind to CD30

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • CD30 is a receptor involved in immune responses.
  • Nuclear factor kappaB (NFkappaB) is a key transcription factor in immunity.

Purpose of the Study:

  • To investigate the interaction between CD30 and tumor necrosis factor receptor-associated factor (TRAF) proteins.
  • To elucidate the role of TRAF2 and TRAF5 in CD30-mediated NFkappaB activation.

Main Methods:

  • Yeast two-hybrid system for interaction analysis.
  • In vitro and in vivo binding assays.
  • Dominant-negative assays using TRAF domains.

Main Results:

  • TRAF2 and TRAF5 directly interact with the D2 subdomain of CD30.
  • Specific amino acid residues in CD30 are critical for TRAF binding.
  • Overexpression of TRAF domains inhibits CD30-induced NFkappaB activation.
  • TRAF2 and TRAF5 mRNA are expressed in CD30-expressing immune cells.

Conclusions:

  • TRAF2 and TRAF5 are key mediators of CD30 signaling.
  • These TRAF proteins directly bind CD30 and activate NFkappaB.
  • The findings reveal a novel mechanism in immune cell activation pathways.

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