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J. Biol. Chem. 275 (45): 35170-35175

© 2000 by The American Society for Biochemistry and Molecular Biology, Inc.

Regulation of Lef-mediated Transcription and p53-dependent Pathway by Associating β-Catenin with CBP/p300*

Makoto Miyagishi{ddagger}§, Ryouji Fujii{ddagger}§, Mitsutoki Hatta{ddagger}§, Eisaku Yoshida§, Natsumi Araya{ddagger}§, Akira Nagafuchi, Satoru Ishihara, Toshihiro Nakajima{ddagger}§, , and Akiyoshi Fukamizu{ddagger}§||

From the {ddagger}Center for Tsukuba Advanced Research Alliance, §Institute of Applied Biochemistry, University of Tsukuba, Tsukuba, Ibaraki 305-8577, and the Department of Cell Biology, Faculty of Medicine, Kyoto University, Kyoto 606-8501, Japan

ABSTRACT Back to Top

Abstract: CBP and its homologue p300 play significant roles in cell differentiation, cell cycle, and anti-oncogenesis. We demonstrated that β-catenin, recently known as a potent oncogene, and CBP/p300 are associated through its CH3 region, which is a primary target of adenoviral oncoprotein E1A and various nuclear proteins, such as p53, cyclin E, and AP-1, and both are colocalized in the nuclear bodies. CBP/p300 potentiated Lef-mediated transactivation of β-catenin, and E1A, a potent inhibitor of CBP/p300, repressed its transactivation. Furthermore, overexpression of stable β-catenin mutant competitively suppressed the p53-dependent pathway. These may be a key mechanism of β-catenin involved in oncogenic events underlying disruption of tumor suppressor function through CBP/p300.

Received for publication April 17, 2000. Revision received July 7, 2000.

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