We previously demonstrated that the cellular ras protooncogene product (Ras) is required for transformation and for the block of adipocytic differentiation by the Simian Virus 40 Large Tumor Antigen (TAg) as well as the Adenovirus E1A (E1A), two viral oncoproteins which are able to bind the Retinoblastoma-susceptibility gene product (Rb) and activate the E2F family of transcription factors. Furthermore, E2F was independently demonstrated to induce the expression of a number of Growth Factor and Receptor genes, which could activate the Ras and Stat3 (signal transducer and activator of transcription-3) pathways. In the present report we examined the activity levels of an effector of Ras, the extracellular-signal-regulated kinase (Erk) as well as Stat3 by Western blotting analysis of serum-starved cells, following expression of TAg and E1A. The results demonstrate that, while TAg expression activates Erk, E1A downregulates Erk expression. On the other hand, both TAg and E1A activate Stat3. These results reveal a profound difference in the activation of these signal transducers, although both viral oncogenes activate E2F.
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