HTLV-1 Tax Enhances NF-κB2 Expression and Binds to the Products p52 and p100, but Does Not Suppress the Inhibitory Function of p100

Abstract

Tax protein of HTLV-1 triggers transcriptional activation through enhancers, NF-κB binding site, 21-bp enhancer, and serum response element. Previously, we demonstrated binding of Tax to transcription factors NF-κBt p105 and p50. Here, we report that Tax enhances expression of HF-κB2 at the mRNA level and proteins; the effect was more apparent on the p52 expression than on its precursor p100, suggesting post-translational regulation. Consistent with these observations, HTLV-1-infected T-cell lines expressed higher levels of p52. Tax binds to the protein products p52 and p100 which inhibits NF-κB proteins forming cytoplasmic complexes; the binding to p100 was preferential over NF-κB1 p105. However, Tax did not induce efficient dissociation of the cytoplasmic complexes p100/c-Rel or p100/p65, and thus did not induce nuclear translocation of c-Rel or p65. This was in sharp contrast to the previous observation that Tax dissociated the p105/c-Rel and IκB-γ/p65 complexes. These results indicate that HTLV-1 Tax interacts with NF-γB2 p100 and p52 and upregulate the NF-κB function, but their contribution to Tax-mediated transcriptional regulation differs from those of NF-κB1. © 1995 Academic Press. All rights reserved.