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An N-terminal inhibitory domain modulates activity of FoxM1 during cell cycle

H J Park1, Z Wang, R H Costa

  • 1Department of Biochemistry and Molecular Genetics (M/C 669), College of Medicine, University of Illinois, Chicago, IL 60607, USA.

Oncogene
|September 25, 2007
PubMed

Insights

The FoxM1 protein

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • FoxM1 is a transcription factor crucial for cell proliferation and mitosis.
  • Its activity is regulated by phosphorylation and growth factors.

Purpose of the Study:

  • To investigate the role of the N-terminal inhibitory domain of FoxM1.
  • To understand how this domain affects FoxM1's transcriptional activity and cell cycle regulation.

Main Methods:

  • Deletion mutagenesis of the FoxM1 N-terminal domain.
  • Assays for transcriptional and transforming activities.
  • Cell cycle analysis and growth factor stimulation experiments.

Main Results:

  • Deleting the N-terminal 232 amino acids of FoxM1 enhances its activity.
  • The N-terminal deletion mutant shows constitutive high activity, independent of cyclin-cdk.
  • The N-terminal domain inhibits FoxM1 activity in G1/S phase cells.

Conclusions:

  • The N-terminal domain of FoxM1 acts as an inhibitor, counteracted by cyclin-cdk phosphorylation.
  • This regulation ensures FoxM1 is fully active during the G2/M phase for mitosis.
  • FoxM1's N-terminal domain plays a key role in cell cycle-dependent gene expression.

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