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o-GlcNAc transferase is activated by CaMKIV-dependent phosphorylation under potassium chloride-induced depolarization

Minseok Song1, Hyeon-Soo Kim, Ji-Man Park

  • 1Department of Life Science, Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, Kyung-Buk 790-784, Republic of Korea.

Cellular Signalling
|November 22, 2007
PubMed

Insights

Potassium chloride-induced depolarization activates O-linked N-acetylglucosamine transferase (OGT) via CaMKIV, enhancing protein O-GlcNAcylation and AP-1 activation in neuronal cells.

Area of Science:

  • Cellular biology
  • Neuroscience
  • Molecular biology

Background:

  • Post-translational modification by O-linked N-acetylglucosamine (o-GlcNAc) regulates protein function.
  • The precise mechanisms controlling o-GlcNAc transferase (OGT) activity are not fully understood.

Purpose of the Study:

  • To investigate the regulation of OGT activity and its role in neuronal signaling.
  • To elucidate the signaling pathway involved in depolarization-induced OGT activation.

Main Methods:

  • Neuronal cell culture (NG-108-15 cells)
  • Potassium chloride-induced depolarization
  • Inhibition of voltage-gated calcium channels and CaMK
  • In vivo and in vitro kinase assays
  • Western blotting
  • Gene expression analysis (AP-1, Timp-1)

Main Results:

  • Depolarization activates OGT and increases protein o-GlcNAcylation in neuronal cells.
  • This activation is dependent on calcium influx and CaMK activity.
  • CaMKIV directly phosphorylates and activates OGT.
  • OGT mediates CaMKIV-dependent activation of AP-1 and subsequent Timp-1 gene expression.

Conclusions:

  • CaMKIV-mediated activation of OGT is a key event in depolarization-induced signaling in neuronal cells.
  • OGT plays a crucial role in the CaMKIV-dependent activation of AP-1 and gene expression under depolarization.

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