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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

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A novel human gene encoding HECT domain and RCC1-like repeats interacts with cyclins and is potentially regulated by

K Mitsui1, M Nakanishi, S Ohtsuka

  • 1Institute of Life Science, Kurume University, 2432-3 Aikawa-machi, Kurume, Fukuoka, 839-0861, Japan.

Biochemical and Biophysical Research Communications
|December 3, 1999
PubMed

Insights

A novel protein, Ceb1, interacts with cyclin-dependent kinases (CDKs) and is elevated when tumor suppressors p53 and RB are inactive. Ceb1 may play a critical role in cell cycle regulation under these conditions.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cyclin E-Cdk2 complex regulates the G1 to S phase transition in the cell cycle.
  • Tumor suppressor proteins p53 and RB are critical regulators of cell cycle progression.
  • Dysregulation of p53 and RB is common in cancer.

Purpose of the Study:

  • To identify novel proteins interacting with cyclin E and its inhibitor p21.
  • To characterize the function and expression of a newly identified protein, Ceb1.
  • To investigate the role of Ceb1 in cell cycle regulation, particularly under conditions of compromised p53 and RB function.

Main Methods:

  • Yeast two-hybrid screening using cyclin E and p21 as bait.
  • Mammalian cell transfection and interaction studies.
  • Expression analysis in various tissues and under different cellular conditions.

Main Results:

  • A novel HECT-family protein with RCC1-like repeats, named Ceb1, was identified.
  • Ceb1 interacts with multiple cyclin subunits of cyclin-dependent kinases (CDKs) in mammalian cells.
  • Ceb1 expression is specific to testis and ovary and is significantly upregulated when p53 and RB functions are impaired.

Conclusions:

  • Ceb1 is a novel CDK-interacting protein with specific expression patterns.
  • Ceb1 expression is induced upon inactivation of tumor suppressors p53 and RB.
  • Ceb1 may play a crucial role in cell cycle progression when CDK activity is elevated due to p53 and RB loss.

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