Cyclin-dependent kinase 5 regulates E2F transcription factor through phosphorylation of Rb protein in neurons

Cell Cycle. 2012 Apr 15;11(8):1603-10. doi: 10.4161/cc.20009. Epub 2012 Apr 15.

Abstract

Recent studies have shown the involvement of cyclin-dependent kinase 5 (Cdk5) in cell cycle regulation in postmitotic neurons. In this study, we demonstrate that Cdk5 and its co-activator p35 were detected in the nuclear fraction in neurons and Cdk5/p35 phosphorylated retinoblastoma (Rb) protein, a key protein controlling cell cycle re-entry. Cdk5/p35 phosphorylates Rb at the sites similar to those phosphorylated by Cdk4 and Cdk2. Furthermore, increased Cdk5 activity elevates activity of E2F transcription factor, which can trigger cell cycle re-entry, leading to neuronal cell death. A normal Cdk5 activity in neurons did not induce E2F activation, suggesting that Cdk5 does not induce cell cycle re-entry under normal conditions. Taken together, these results indicate that Cdk5 can regulate cell cycle by its ability to phosphorylate Rb. Most importantly, increased Cdk5 activity induces cell cycle re-entry, which is especially detrimental for survival of postmitotic neurons.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cyclin-Dependent Kinase 5 / deficiency
  • Cyclin-Dependent Kinase 5 / genetics
  • Cyclin-Dependent Kinase 5 / metabolism*
  • E2F Transcription Factors / metabolism*
  • Mass Spectrometry
  • Mice
  • Molecular Sequence Data
  • Nerve Tissue Proteins / deficiency
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Neurons / metabolism*
  • Phosphopeptides / analysis
  • Phosphorylation
  • Retinoblastoma Protein / metabolism*

Substances

  • E2F Transcription Factors
  • Nerve Tissue Proteins
  • Phosphopeptides
  • Retinoblastoma Protein
  • neuronal Cdk5 activator (p25-p35)
  • Cyclin-Dependent Kinase 5