The aryl hydrocarbon nuclear translocator alters CD30-mediated NF-kappaB-dependent transcription.

Journal Article (Journal Article)

Expression and signaling of CD30, a tumor necrosis factor receptor family member, is up-regulated in numerous lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma. To gain insight into the mechanism of CD30 signaling, we used an affinity purification strategy that led to the identification of the aryl hydrocarbon receptor nuclear translocator (ARNT) as a CD30-interacting protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor kappaB (NF-kappaB). ALCL cells that were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, whereas RelA recruitment to the same sites was potentiated, resulting in the augmented expression of these NF-kappaB-responsive genes. These findings indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.

Full Text

Duke Authors

Cited Authors

  • Wright, CW; Duckett, CS

Published Date

  • January 9, 2009

Published In

Volume / Issue

  • 323 / 5911

Start / End Page

  • 251 - 255

PubMed ID

  • 19131627

Pubmed Central ID

  • PMC2682336

Electronic International Standard Serial Number (EISSN)

  • 1095-9203

Digital Object Identifier (DOI)

  • 10.1126/science.1162818


  • eng

Conference Location

  • United States