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Updated: Jun 26, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Cyclin-dependent kinase-3-mediated c-Jun phosphorylation at Ser63 and Ser73 enhances cell transformation

Yong-Yeon Cho1, Faqing Tang, Ke Yao

  • 1The Hormel Institute, University of Minnesota, 801 16th Avenue Northeast, Austin, MN 55912, USA.

Cancer Research
|January 2, 2009
PubMed

Insights

Cyclin-dependent kinase (Cdk) 3 phosphorylates c-Jun, a key component of the activator protein-1 (AP-1) complex. This Cdk3/c-Jun pathway is vital for epidermal growth factor (EGF)-stimulated cell proliferation and transformation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • c-Jun is a critical component of the activator protein-1 (AP-1) complex.
  • AP-1 regulates gene expression, cell proliferation, transformation, and cancer development.

Purpose of the Study:

  • To identify novel kinases that phosphorylate c-Jun.
  • To investigate the role of cyclin-dependent kinase (Cdk) 3 in c-Jun activation and downstream signaling.

Main Methods:

  • In vitro and ex vivo kinase assays using Cdk3, Cdk2, and c-Jun NH(2)-terminal kinase.
  • Epidermal growth factor (EGF) stimulation of cells.
  • Analysis of AP-1 transactivation.
  • Ectopic expression of Cdk3 in JB6 Cl41 and NIH3T3 cells.

Main Results:

  • Cdk3, but not Cdk2 or c-Jun NH(2)-terminal kinase, was identified as a novel kinase of c-Jun.
  • Cdk3 phosphorylated c-Jun at Ser63 and Ser73.
  • EGF-induced Cdk3 activation led to c-Jun phosphorylation and enhanced AP-1 transactivation.
  • Ectopic Cdk3 expression promoted EGF-induced anchorage-independent cell transformation and Ras(G12V)-stimulated foci formation.

Conclusions:

  • The Cdk3/c-Jun signaling axis is a novel pathway involved in EGF-stimulated cell proliferation.
  • Cdk3 plays a significant role in EGF-induced cell transformation through AP-1 activation.

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