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The Aryl Hydrocarbon Nuclear Translocator Alters CD30-Mediated NF-B–Dependent Transcription
Casey W. Wright1*, and
Colin S. Duckett1,2
Abstract:
Expression and signaling of CD30, a tumor necrosis factor receptorfamily member, is up-regulated in numerous lymphoid-derivedneoplasias, most notably anaplastic large-cell lymphoma (ALCL)and Hodgkin's lymphoma. To gain insight into the mechanism ofCD30 signaling, we used an affinity purification strategy thatled to the identification of the aryl hydrocarbon receptor nucleartranslocator (ARNT) as a CD30-interacting protein that modulatedthe activity of the RelB subunit of the transcription factornuclear factor B (NF-B). ALCL cells that were deficient in ARNTexhibited defects in RelB recruitment to NF-B–responsivepromoters, whereas RelA recruitment to the same sites was potentiated,resulting in the augmented expression of these NF-B–responsivegenes. These findings indicate that ARNT functions in concertwith 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 atAustin, 1 University Station A1915, Austin, TX 78712, USA.
To whom correspondence should be addressed. E-mail: colind{at}umich.edu
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B–Dependent Transcription
B (NF-
To whom correspondence should be addressed. E-mail: 
