The analysis of the MCMV IE enhancer revealed the presence of many putative binding sites for the transcription factors AP-1 and NFkB. Previous studies suggested that such factors represent a final target for the metabolic cascade triggered by serum and growth factors. On these basis we wanted to verify if serum stimulates the transcriptional activity of the MCMV IE enhancer through p21ras and AP-1 and NFkB according to the actual model of transduction of the mitogenic signal. Our data demonstrate that serum stimulates the MCMV IE enhancer through a pathway in which the p21ras is involded, as demonstrated by using the dominant inhibitory mutant ras(Asn 17). Moreover deletion mutant analysis of the enhancer showed that the serum responsive region lies between nucleotides -1280 and -285 and contains a high concentration of putative AP-1 and NFkB binding sites.
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