Role of E2F1 in Endoplasmic Reticulum Stress Signaling

  • Park, Kyung Mi (Functional Genomics Research Center, Division of Molecular Therapeutics, Korea Research Institute of Bioscience and Biotechnology) ;
  • Kim, Dong Joon (Functional Genomics Research Center, Division of Molecular Therapeutics, Korea Research Institute of Bioscience and Biotechnology) ;
  • Paik, Sang Gi (Department of Biology, Chungnam National University) ;
  • Kim, Soo Jung (Functional Genomics Research Center, Division of Molecular Therapeutics, Korea Research Institute of Bioscience and Biotechnology) ;
  • Yeom, Young Il (Functional Genomics Research Center, Division of Molecular Therapeutics, Korea Research Institute of Bioscience and Biotechnology)
  • Received : 2005.11.25
  • Accepted : 2006.03.29
  • Published : 2006.06.30

Abstract

The transcription factor E2F1 coordinates cell cycle progression and induces apoptosis in response to DNA damage stress. Aside from DNA damage, the role of E2F1 in the endoplasmic reticulum (ER) stress signaling pathways is unclear. We found that $E2F1^{-/-}$ murine embryonic fibroblasts (MEFs) are resistant to apoptosis triggered by the ER stress inducer thapsigargin. In addition, E2F1 deficiency results in enhanced phosphorylation of eukaryotic translation initiation factor $2{\alpha}$ ($elF2{\alpha}$). These results therefore indicate that E2F1 deficiency increases phosphorylation of $elF2{\alpha}$ in response to ER stress triggered by thapsigargin, and suggest that the reduction in ER stress-induced apoptosis in E2F1-deficient cells is related to the high level of $elF2{\alpha}$ phosphorylation.

Keywords

Acknowledgement

Supported by : Korean Ministry of Science and Technology

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