Tumor necrosis factor alpha induces the adenovirus early 3 promoter by activation of NF-kappaB.

The Journal of Biological Chemistry
F Deryckere, H G Burgert

Abstract

The early transcription unit 3 (E3) of human adenoviruses encodes proteins which appear to subvert host defense mechanisms. For example, the E3/19K protein inhibits the transport of major histocompatibility complex (MHC) class I molecules to the cell surface and thereby prevents cell lysis by cytotoxic T cells. Tumor necrosis factor alpha (TNF) stimulates expression of MHC molecules on the cell surface of normal cells but not of E3(+) cells, rather, a further reduction of MHC expression is evident. This was attributed to the increased expression of E3/19K upon TNF treatment, an effect also observed for other E3 proteins. We investigated the mechanism of the TNF-mediated up-regulation of E3 products. We show that TNF stimulates expression of a luciferase reporter gene driven by the E3 promoter. Mutation of individual transcription factor binding sites within the E3 promoter reveals the importance of the NF-kappaB binding site kappa2 for TNF inducibility. Electrophoretic mobility shift assays using antibodies directed against various members of the NF-kappaB family demonstrate that stimulation by TNF is mediated by the p50-p65 NF-kappaB complex. TNF inducibility does not depend on coexpression of E1A and can be observed during in...Continue Reading

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