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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Physical and functional interactions between Pim-1 kinase and Cdc25A phosphatase. Implications for the Pim-1-mediated

T Mochizuki1, C Kitanaka, K Noguchi

  • 1Biophysics Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.

The Journal of Biological Chemistry
|June 22, 1999
PubMed

Insights

The pim-1 oncogene (Pim-1) kinase phosphorylates Cdc25A, a cell cycle phosphatase. This interaction links Pim-1 and c-Myc, impacting cell growth and apoptosis.

Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Oncogenesis

Background:

  • The pim-1 oncogene encodes a serine/threonine kinase (Pim-1) crucial for cytokine signaling and cell proliferation.
  • Pim-1 cooperates with c-Myc in oncogenesis and apoptosis, but its downstream effectors are unknown.
  • Understanding Pim-1's molecular basis is essential for deciphering its role in cell signaling.

Purpose of the Study:

  • To identify the downstream effector molecule(s) of Pim-1 kinase.
  • To investigate the interaction between Pim-1 and Cdc25A.
  • To elucidate the role of Cdc25A as a mediator of Pim-1 function.

Main Methods:

  • In vitro and in vivo interaction studies between Pim-1 and Cdc25A.
  • Assessment of Pim-1-mediated phosphorylation of Cdc25A.
  • Enzyme activity assays for Cdc25A phosphatase activity.
  • Cellular transformation and apoptosis assays using wild-type and kinase-inactive Pim-1.

Main Results:

  • Pim-1 physically interacts with Cdc25A.
  • Pim-1 phosphorylates Cdc25A, enhancing its phosphatase activity.
  • Wild-type Pim-1 promotes Cdc25A-mediated cellular transformation and apoptosis, unlike kinase-inactive Pim-1.

Conclusions:

  • Cdc25A is a substrate and effector for Pim-1 kinase.
  • Cdc25A acts as a molecular link between Pim-1 and c-Myc.
  • Pim-1 signaling converges on the cell cycle machinery via Cdc25A phosphorylation.

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