Abstract
A nuclear component interacting with a retinoic acid re-sponse element (RARE-β) derived from the all-trans-retinoic acid recep-tor β (RARβ) gene promoter was detected in the rat liver by gel-shift assay. Competition experiments using the competitors of the other retinoid response elements and non-specific sequences upon the binding of this hepatic component (HBC) to the RARE-β revealed that the binding of the HBC to the RARE-β was competed only by the self competitor, but not the other elements, suggesting that the HBC is specific for the RARE-β. Moreover, although the specific monoclonal antibodies for RARα, RARβ, and RARγ reacted and shifted up the DNA complexes of endogenous as well as recombinant RARs, the DNA complex with HBC was not subjected to the immunoreaction with the antibodies. Thus, newly identified HBC, which is distinct from the characterized retinoid receptors, may modulate retinoid signaling through its direct binding upon the RARE-β.
