Oncogene activation of HIV-LTR-driven expression via the NF-kappa B binding sites.
The Raf-1 proto-oncogene product is a highly regulated serine/threonine kinase that functions in signal transduction downstream from growth factor receptors and upstream from nuclear proto-oncogene products. Using a transient cotransfection assay we have found that activated Raf-1 activates expression from the HIV-LTR. Analysis of a series of 5' deletion and point mutations revealed the NF-kappa B motifs as the Raf-responsive element in the HIV-LTR. Moreover, Raf-BXB activated expression from heterologous promoters driven by the HIV NF-kappa B binding sites. In addition to Raf, we show that v-Src, v-H-Ras and v-Mos activate HIV-LTR expression through the NF-kappa B binding sites and v-H-Ras- induced HIV-LTR expression is mediated by Raf-1. These findings may have implications for the involvement of the cellular homologues of these oncogenes in the switch from latent to productive infection by HIV in response to T-cell activation.[1]References
- Oncogene activation of HIV-LTR-driven expression via the NF-kappa B binding sites. Bruder, J.T., Heidecker, G., Tan, T.H., Weske, J.C., Derse, D., Rapp, U.R. Nucleic Acids Res. (1993) [Pubmed]
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