The oncogenicity of Jun.

A mutational analysis of the delta region of the Jun protein shows an inverse correlation between transforming and transactivation potential of the mutant proteins if both properties are measured in chicken embryo fibroblasts. The possibility that Jun acquires oncogenicity not by gain but by loss of function is also suggested by the down regulation of the differentiation control element MyoD by Jun and by the low transactivating potential of highly transforming chimeric proteins of Jun and JunD and Jun and herpes simplex VP16. These observations raise questions concerning the relative importance of positive and negative transcriptional control signals imitated by Jun.