Human T‐cell leukemia virus type 1 Tax protein stimulates the interferon‐responsive enhancer element via NF‐κB activity¹

Abstract

Gene expression in Rat-1 fibroblast cells transformed by Tax from human T-cell leukemia virus type 1 was studied using the reverse transcriptase polymerase chain reaction differential display technique. The analysis revealed eight genes that were upregulated and one gene that was suppressed in Tax-transformed cells. Interestingly, at least four of the upregulated genes were interferon-stimulated genes. Promoter analysis of the 2',5'-oligoadenylate synthetase gene, which was activated in both Tax-transformed Rat-1 cells and primary adult T-cell leukemia cells, demonstrated that Tax indirectly activates its interferon-responsive enhancer element in a nuclear factor-kappaB pathway-dependent manner, indicating a close association of interferon signaling with the transformation by Tax.

Human T‐cell leukemia virus type‐I oncoprotein Tax inhibits Fas‐mediated apoptosis by inducing cellular FLIP through activation of NF‐κB

“…Tax mutant M22 activates the transcriptional activity of CREB/ATF1 but not NF‐κB, while another Tax mutant d3 can activate NF‐κB but exert little affects on CREB/ATF1 (Fig. 7C,D) (Shimizu et al . 2003).…”

“…Wild‐type Tax, its mutants M22 and d3, and the dominant negative NF‐κB (DNp50: the truncated mutant of NF‐κB p105) were expressed using the vector pCG (Shimizu et al . 2003).…”

Mechanism of Action of Inhibition of Allergic Immune Responses by a Novel Antedrug TLR7 Agonist

“…IL-5 or eotaxin in the BAL fluid and supernatant of the OVA-stimulated MLN cells was measured by ELISA kit, following the manufacturer's instructions. type I IFN-inducible 29,59-oligoadenylate synthetase gene (L929/2,5-OAS), as described previously (29). The luciferase reporter plasmids were constructed by inserting human 29,59-oligoadenylate synthetase promoter fragments (21262 to +108), which were isolated by PCR of human placenta genomic DNA (Oncor, Gaithersburg, MD), into the multicloning site of pGL3-basic plasmid (Promega).…”

Transformation of SV40-immortalized human uroepithelial cells by 3-methylcholanthrene increases IFN- and Large T Antigen-induced transcripts

“…In addition, studies of infectious diseases (scrapie, herpes simplex virus type 1, human cytomegalovirus, human influenza virus C, type 1 diabetes) have linked IFN-γ inducible gene expression with the presence of disease and/or anti-viral mechanisms [42-45]. In a recent study employing HTLV-1 to transform Rat-1 fibroblast cells in vitro , four of eight up regulated genes were IFN-stimulated genes, and the 2',5'-OAS promoter was activated by viral Tax indirectly through an NFκB-dependent pathway, linking IFN-signaling with Tax transformation [46]. We observed evidence of PKR up-regulation, which can directly activate the NFκ-B pathway.…”