Abstract
The Tax oncoprotein promotes cellular transformation and is associated with the pathogenesis of adult T-cell leukemia. Tax expression activates transcription via the cAMP enhancer binding protein/activating transcription factor (CREB/ATF) and NF-kappaB pathways. In contrast to its positive action, here we demonstrate that Tax is a potent repressor of steroid and retinoid receptor transcription. The Tax protein becomes localized in the promyelocytic (PML) oncogenic domain, and unexpectedly, expression of the PML protein reverses Tax-induced repression. These results suggest that PML and Tax may act in opposing manners to influence nuclear receptor transcription and human T-cell leukemia retrovirus pathogenesis.