Takahashi, Akiko, Higashino, Fumihiro, Aoyagi, Mariko, Nakayama, Masayuki, Yanagawa, Aya, Hasegawa, Hiroichi, Hatta, Mitsutoki, Ishida, Setsuko, Nakajima, Koichi, Totsuka, Yasunori, and Shindoh, Masanobu
Abstract: E1AF was first identified as a transcription factor that binds to enhancer motifs of the adenovirus E1A gene and is thought to be a human homologue of mouse PEA3, one of the ets oncoprotein families. Here we show the effect of E1A on the gene expression and function of E1AF. E1A repressed the activity of E1AF promoter, and the N-terminal region of E1A, which is involved in the oncogenic activity of E1A, was essential for this repression. The ability as a transcription factor of E1AF, as well as those of the other PEA3 subfamily members ER81 and ERM, was also repressed by E1A via the same oncogenic domain. Furthermore, E1AF repressed the transformation activity of E1A cooperating with E1B, whereas the other ets family Ets-1 enhanced this activity. These results suggest that E1AF is one of the targets of E1A. [Copyright &y& Elsevier]