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 journalArticle

21 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

Fingerprint

Presenilins
Fibroblasts
Mitogen-Activated Protein Kinase Kinases
Notch Receptors
Amyloid beta-Protein Precursor
Null Lymphocytes
Cell death
Transcription
Mitogen-Activated Protein Kinases
Cells
Apoptosis
Cell Death
Down-Regulation
Processing

Keywords

  • Mitogen-activated protein kinase
  • Presenilin
  • Signal transduction

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Presenilin acts as a positive regulator of basal level activity of ERK through the Raf-MEK1 signaling pathway. / Kim, Mi Yeon; Park, Ji Hye; Choi, Eui Ju; Park, Hee Sae.

In: Biochemical and Biophysical Research Communications, Vol. 332, No. 2, 01.07.2005, p. 609-613.

Research output: Contribution to journalArticle

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