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Science 323 (5911): 251-255

Copyright © 2009 by the American Association for the Advancement of Science

The Aryl Hydrocarbon Nuclear Translocator Alters CD30-Mediated NF-{kappa}B–Dependent Transcription

Casey W. Wright1*, and Colin S. Duckett1,2{dagger}

Abstract: 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 {kappa}B (NF-{kappa}B). ALCL cells that were deficient in ARNT exhibited defects in RelB recruitment to NF-{kappa}B–responsive promoters, whereas RelA recruitment to the same sites was potentiated, resulting in the augmented expression of these NF-{kappa}B–responsive genes. These findings indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.

1 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
2 Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

* Present address: College of Pharmacy, University of Texas at Austin, 1 University Station A1915, Austin, TX 78712, USA.

{dagger} To whom correspondence should be addressed. E-mail: colind{at}umich.edu


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