Presenilin acts as a positive regulator of basal level activity of ERK through the Raf-MEK1 signaling pathway

Mi Yeon Kim, Ji Hye Park, Eui Ju Choi, Hee Sae Park

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

Presenilins (PS) have been reported to be functionally involved in amyloid precursor protein processing, notch receptor signaling, and programmed cell death, or apoptosis. To understand the role of PS1 in the signaling events, we investigated in this study the role of PS1 in the basal level of mitogen-activated protein kinase (MAPK) pathways using PS1-/- mouse embryonic fibroblast (MEF) cells from PS1-null mice. Interestingly, the basal level of ERK activity, but not JNK or p38 activity, is lower in PS1 -/- MEF cells than in PS1+/+ MEF cells. In PS1 -/- MEF cells, the basal activities of Raf and MEK, the upstream signaling component of ERK, are also lower than in PS1+/+ MEF cells. Furthermore, Elk-1 transcription activity also down-regulates in PS1 -/- MEF cells. Collectively, our data suggest that PS can modulate the basal level of ERK activity through the Raf-MEK-dependent pathway.

Original languageEnglish
Pages (from-to)609-613
Number of pages5
JournalBiochemical and biophysical research communications
Volume332
Issue number2
DOIs
Publication statusPublished - 2005 Jul 1

Bibliographical note

Funding Information:
This research was supported by a grant (M103KV010004-03K2201-00400) from the Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology (H.-S. Park), and Korea Research Foundation grant (C00026), the Republic of Korea.

Keywords

  • Mitogen-activated protein kinase
  • Presenilin
  • Signal transduction

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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