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DEK is a poly(ADP-ribose) acceptor in apoptosis and mediates resistance to genotoxic stress

F Kappes1, J Fahrer, M S Khodadoust

  • 1University of Konstanz, Department of Biology, Box X911, D-78457 Konstanz, Germany.

Molecular and Cellular Biology
|March 12, 2008
PubMed

Insights

The DEK protein, involved in cancer and immunity, protects cells from DNA damage. Modifications during cell death release DEK, where it

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Immunology

Background:

  • DEK is a nuclear phosphoprotein crucial for chromatin structure, implicated in oncogenesis and autoimmunity.
  • The regulation of DEK's DNA binding and its diverse functions in DNA/RNA processes are not fully understood.
  • Altered DEK phosphorylation during apoptosis suggests a role in stress signaling.

Purpose of the Study:

  • To investigate the posttranslational modifications of DEK during apoptosis.
  • To determine DEK's role in DNA repair and cellular protection against genotoxic stress.
  • To explore the extracellular function and autoantigenic properties of modified DEK.

Main Methods:

  • Analysis of DEK phosphorylation and poly(ADP-ribosyl)ation in apoptotic cells.
  • Gene silencing techniques to assess DEK's function in DNA repair and genotoxicity.
  • Detection of extracellular DEK and autoantibodies in patient samples.

Main Results:

  • DEK undergoes extensive phosphorylation and poly(ADP-ribosyl)ation during apoptosis.
  • DEK promotes DNA lesion repair and protects cells from genotoxic agents.
  • Modified DEK is released extracellularly and recognized by autoantibodies in juvenile idiopathic arthritis patients.

Conclusions:

  • Poly(ADP-ribosyl)ation significantly influences DEK's autoantigenic properties and cell survival functions.
  • DEK plays a critical role in cellular defense against DNA damage.
  • Extracellular modified DEK may serve as a biomarker in autoimmune diseases like juvenile idiopathic arthritis.

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