Roland M. Schmid

TL;DR: It is shown that an interaction between NF‐kappa B and Sp1 is required for inducible HIV‐1 gene expression and may serve as a regulatory mechanism to activate specific viral and cellular genes.

TL;DR: P49 acts in synergy with p65 to stimulate the human immunodeficiency virus (HIV) enhancer in transiently transfected Jurkat cells, suggesting p49/plOO NF-κB could be important in the regulation of HIV and other κB-containing genes.

TL;DR: Transactivation mediated by the p49/p100 and p65 NF-kappa B proteins is sensitive to minor changes in the sequence of the kappa B site, providing a mechanism to selectively regulate variant kappaB sites associated with different cellular and viral genes.

TL;DR: The data suggest that binding of the NF KB2 subunit to the HIV enhancer is facilitated by RelA(p65) and that this NFKB2(p49)/p65 heterodimeric complex mediates transcriptional activation which is subject to regulation by MAD-3.

TL;DR: The genomic structure and sequence of NF-kappa B2 revealed the presence of two promoters and at least four kappa B regulatory elements, which mediate responsiveness to phorbol myristate acetate and tumor necrosis factor alpha, and it is demonstrated that a novel mode of k Kappa B-dependent regulation is mediated by specific kappaB sites in the NFKB2 promoter.