Cyclin E/Cdk2, P/CAF, and E1A regulate the transactivation of the c-myc promoter by FOXM1

Biochemical and Biophysical Research Communications
Inken Wierstra, Jürgen Alves

Abstract

FOXM1c transactivates the c-myc promoter by binding directly to its TATA-boxes. The present study demonstrates that the transactivation of the c-myc promoter by FOXM1c is enhanced by the key proliferation signal cyclin E/Cdk2, but repressed by P/CAF and the adenoviral oncoprotein E1A. Furthermore, FOXM1c interacts with the coactivator and histone acetyltransferase P/CAF. This study shows that, on the c-myc-P1 TATA-box, FOXM1c does not function simply as normal transcription factor just binding to an unusual site. Moreover, the inhibitory N-terminus of FOXM1c does not inhibit its transrepression domain or its EDA. Others reported that a cyclin/Cdk-binding LXL-motif of the splice variant FoxM1b is required for its interaction with Cdk2, Cdk1, and p27, its phosphorylation by Cdk1 and its activation by Cdc25B. In contrast, we now demonstrate that this LXL-motif is not required for the activation of FOXM1c by cyclin D1/Cdk4, cyclin E/Cdk and cyclin A/Cdk2 or for the repression of FOXM1c by p27.

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Citations

Jan 22, 2013·Biochemical and Biophysical Research Communications·Inken Wierstra
Dec 22, 2009·Cancer Treatment Reviews·Zhiwei WangFazlul H Sarkar
Aug 31, 2011·Biochemical and Biophysical Research Communications·Inken Wierstra
Aug 24, 2011·Nature Chemistry·Nagaratna S HegdeShankar Balasubramanian
Feb 13, 2021·Nature Biotechnology·Daniel S C ButlerCatharina Svanborg
Jul 30, 2021·World Journal of Methodology·Xin-Yu Zeng, Ming Li

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