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J. Biol. Chem., Vol. 277, Issue 42, 39769-39776, October 18, 2002

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p73 Independent of c-Myc Represses Transcription of Platelet-derived Growth Factor -Receptor through Interaction with NF-Y^*

Anders Hackzell, Hidetaka Uramoto, Hiroto Izumi^§, Kimitoshi Kohno^§, and Keiko Funa^¶

From the  Department of Cell Biology, Institute of Anatomy and Cell Biology, Göteborg University, Box 420, SE-405 30 Gothenburg, Sweden and the ^§ Department of Molecular Biology, University of Occupational and Environmental Health School of Medicine, Kitakyushu 807, Japan

We recently reported that c-Myc represses the transcription of platelet-derived growth factor (PDGF) -receptor (Izumi, H., Molander, C., Penn, L. Z., Ishisaki, A., Kohno, K., and Funa, K. (2001) J. Cell Sci. 114, 1533-1544). We demonstrate here that the p53 family protein p73 represses PDGF -receptor transcription essentially by the same mechanism. p73 but not p73 or p53 represses the transcription in concordance with its ability to bind NF-YC and NF-YB. None of other p73 isoforms (i.e. p73, p73, p73), C-terminal deletion mutants of p73, and p53 is able to bind NF-Y with the exception of p63. This finding suggests that the sterile -motif domain present only in p73 and p63 is the interaction site. For the repression, the N-terminal transactivation domain of p73 is also indispensable, arguing for the importance of the activity of p73 in the mechanism. p73 binds the C-terminal HAP domain of NF-YC previously found to be the interaction site with c-Myc and TBP. Because c-Myc induces and activates p73 (Zaika, A., Irwin, M., Sansome, C., and Moll, U. M. (2001) J. Biol. Chem. 276, 11310-11316) and they bind each other (Uramoto, H., Izumi, H., Ise, T., Tada, M., Uchiumi, T., Kuwano, M., Yasumoto, K., Funa, K., and Kohno, K. (2002) J. Biol. Chem. 277, in press), we examined whether the repression by p73 is dependent on c-Myc. However, Myc-null rat fibroblasts are also susceptible to p73-induced repression. Serum stimulation of NIH3T3 cells gradually decreased the amount of endogenous NF-Y binding to the PDGF -receptor promoter, whereas NF-YA expression in the nuclear extracts remains unchanged. Our results indicate that serum stimulation induces c-Myc and p73, leading to the down-regulation of PDGF -receptor expression by repressing its transcription.

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