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Transcriptional regulation of 1-cys peroxiredoxin by the proto-oncogene protein DEK

Dong-Wook Kim1, Ji-Young Kim, Sulji Choi

  • 1Department of Biomedical Science, College of Life Science, CHA University, Seongnam 463-836, Korea.

Molecular Medicine Reports
|April 8, 2011
PubMed

Insights

The nuclear phosphoprotein DEK negatively regulates 1-cys peroxiredoxin (1-cys Prx) transcription. This repression is enhanced by the NF-κB subunit p65, revealing a novel mechanism of gene regulation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Biology

Background:

  • The nuclear phosphoprotein DEK is implicated in various diseases, including leukemia and autoimmune disorders.
  • DEK possesses acidic domains and inhibits histone acetyltransferase activity by binding to histones.
  • Previous studies identified 1-cys peroxiredoxin (1-cys Prx) as upregulated under DEK knockdown.

Purpose of the Study:

  • To investigate the regulatory relationship between DEK and 1-cys Prx transcription.
  • To elucidate the role of NF-κB subunit p65 in DEK-mediated gene regulation.

Main Methods:

  • Utilized in vivo reporter assays with short hairpin RNA (shRNA) for DEK knockdown.
  • Analyzed protein recruitment to the 1-cys Prx promoter region.
  • Investigated the synergistic effect of DEK and p65 on gene transcription.

Main Results:

  • DEK was confirmed to negatively regulate 1-cys Prx transcription.
  • The NF-κB subunit p65 demonstrated a synergistic effect on DEK-mediated repression.
  • Both DEK and p65 were found to be recruited to the 1-cys Prx promoter.

Conclusions:

  • DEK plays a significant role in the transcriptional regulation of 1-cys Prx.
  • Protein interactions, specifically between DEK and NF-κB p65, are crucial for modulating target gene transcription.
  • This study reveals a novel mechanism of DEK-mediated transcriptional control involving protein cooperation.

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