TRAF2-Mediated Activation of NF-κB by TNF Receptor 2 and CD40

DOI Web Site 31 Citations
  • Mike Rothe
    Molecular Biology Department, Tularik, Inc., South San Francisco, CA 94080, USA.
  • Vidya Sarma
    Department of Pathology, University of Michigan Medical School, Ann Arbor, Ml 48109-0602, USA.
  • Vishva M. Dixit
    Department of Pathology, University of Michigan Medical School, Ann Arbor, Ml 48109-0602, USA.
  • David V. Goeddel
    Molecular Biology Department, Tularik, Inc., South San Francisco, CA 94080, USA.

Abstract

<jats:p>TNF receptor-associated factor (TRAF) proteins are candidate signal transducers that associate with the cytoplasmic domains of members of the tumor necrosis factor (TNF) receptor superfamily. The role of TRAFs in the TNF-R2 and CD40 signal transduction pathways, which result in the activation of transcription factor NF-κB, was investigated. Overexpression of TRAF2, but not TRAF1 or TRAF3, was sufficient to induce NF-κB activation. A truncated derivative of TRAF2 lacking an amino-terminal RING finger domain was a dominant-negative inhibitor of NF-κB activation mediated by TNF-R2 and CD40. Thus, TRAF2 is a common mediator of TNF-R2 and CD40 signaling.</jats:p>

Journal

  • Science

    Science 269 (5229), 1424-1427, 1995-09-08

    American Association for the Advancement of Science (AAAS)

Citations (31)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top