The Aryl Hydrocarbon Nuclear Translocator Alters CD30-Mediated NF-
B–Dependent Transcription
Casey W. Wright1* and
Colin S. Duckett1,2
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
B (NF-
B). ALCL cells that were deficient in ARNT
exhibited defects in RelB recruitment to NF-
B–responsive
promoters, whereas RelA recruitment to the same sites was potentiated,
resulting in the augmented expression of these NF-
B–responsive
genes. These findings indicate that ARNT functions in concert
with RelB in a CD30-induced negative feedback mechanism.
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.
To whom correspondence should be addressed. E-mail: colind{at}umich.edu
