Depletion of the AP-1 repressor JDP2 induces cell death similar to apoptosis

M. Lerdrup, C. Holmberg, N. Dietrich, E. Shaulian, T. Herdegen, M. Jäättelä, T. Kallunki*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

JDP2 is a ubiquitously expressed nuclear protein that efficiently represses the activity of the transcription factor AP-1. Thus far, all studies of JDP2 function have relied on the ectopic expression of the protein. In this study, we use a different approach: depletion of JDP2 from cells. Specific depletion of JDP2 resulted in p53-independent cell death that resembles apoptosis and was evident at 72 h. The death mechanism was caspase dependent as the cells could be rescued by treatment with caspase inhibitor zVAD. Our studies suggest that JDP2 functions as a general survival protein, not only following UV-irradiation, as reported earlier, but also under normal culture conditions. Thus, our data support that JDP2 is a cellular survival protein whose presence is necessary for normal cellular function.

Original languageAmerican English
Pages (from-to)29-37
Number of pages9
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Volume1745
Issue number1
DOIs
StatePublished - 15 Aug 2005

Bibliographical note

Funding Information:
We acknowledge Birgit Poulsen for help with the plasmid isolation. This work was supported by grants from Novo Nordisk Foundation, Danish Cancer Research Foundation, Danish Cancer Society, Research Foundation of Leo Pharmaceuticals as well as Bøje Benzon Stipend of Alfred Benzon Foundation (all to T.K.), the Henselt Foundation of the University of Kiel (C.H. and T.H.) and the Deutsche Forschungsgemeinschaft -supported SFB 415 (C.H. and T.H.).

Keywords

  • AP-1
  • Antisense
  • Caspase
  • JDP2
  • Programmed cell death

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