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

doi:10.1016/j.bbrc.2005.05.001

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 journal › Article › peer-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 language	English
Pages (from-to)	609-613
Number of pages	5
Journal	Biochemical and biophysical research communications
Volume	332
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2005.05.001
Publication status	Published - 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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10.1016/j.bbrc.2005.05.001

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

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.",

keywords = "Mitogen-activated protein kinase, Presenilin, Signal transduction",

author = "Kim, {Mi Yeon} and Park, {Ji Hye} and Choi, {Eui Ju} and Park, {Hee Sae}",

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.",

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AU - Park, Ji Hye

AU - Choi, Eui Ju

AU - Park, Hee Sae

N1 - 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.

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N2 - 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.

AB - 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.

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

Abstract

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