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I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction.

Authors:
Rothe M, Xiong J, Shu HB, Williamson K, Goddard A, Goeddel DV
Affiliation:
Journal:
Proceedings of the National Academy of Sciences of the United States of America

Abstract

Tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins associate with and transduce signals from TNF receptor 2, CD40, and presumably other members of the TNF receptor superfamily. TRAF2 is required for CD40- and TNF-mediated activation of the transcription factor NF-kappa B. Here we describe the isolation and characterization of a novel TRAF-interacting protein, I-TRAF, that binds to the conserved TRAF-C domain of the three known TRAFs. Overexpression of I-TRAF inhibits TRAF2-mediated NF-kappa B activation signaled by CD40 and both TNF receptors. Thus, I-TRAF appears as a natural regulator of TRAF function that may act by maintaining TRAFs in a latent state.

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