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Tumor necrosis factor receptor-associated factor (TRAF)2 represses the T helper cell type 2 response through interaction with NFAT-interacting protein (NIP45)

Academic Article
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Overview

authors

  • Lieberson, R.
  • Mowen, Kerri
  • McBride, K. D.
  • Leautaud, V.
  • Zhang, X. K.
  • Suh, W. K.
  • Wu, L.
  • Glimcher, L. H.

publication date

  • July 2001

journal

  • Journal of Experimental Medicine  Journal

abstract

  • Recently we have identified a novel protein NIP45 (nuclear factor of activated T cells [NFAT]-interacting protein) which substantially augments interleukin (IL)-4 gene transcription. The provision of NIP45 together with NFAT and the T helper cell type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, such as B cells or Th1 clones, results in substantial IL-4 secretion to levels that approximate those produced by primary Th2 cells. In studies designed to further our understanding of NIP45 activity, we have uncovered a novel facet of IL-4 gene regulation. We present evidence that members of the tumor necrosis factor receptor-associated factor (TRAF) family of proteins, generally known to function as adapter proteins that transduce signals from the tumor necrosis factor receptor superfamily, contribute to the repression of IL-4 gene transcription and that this effect is mediated through their interaction with NIP45.

subject areas

  • Animals
  • CD4-Positive T-Lymphocytes
  • Carrier Proteins
  • Interleukin-4
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Mice, Transgenic
  • Nuclear Proteins
  • Promoter Regions, Genetic
  • Proteins
  • Receptors, Tumor Necrosis Factor
  • T-Lymphocytes, Helper-Inducer
  • TNF Receptor-Associated Factor 2
  • Th2 Cells
  • Transcription, Genetic
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Research

keywords

  • NIP45
  • TRAF2
  • cytokines
  • interleukin-4
  • transcription
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Identity

PubMed Central ID

  • PMC2193447

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.194.1.89

PubMed ID

  • 11435475
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Additional Document Info

start page

  • 89

end page

  • 98

volume

  • 194

issue

  • 1

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