TY - JOUR
T1 - Presenilin acts as a positive regulator of basal level activity of ERK through the Raf-MEK1 signaling pathway
AU - Kim, Mi Yeon
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.
PY - 2005/7/1
Y1 - 2005/7/1
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.
KW - Mitogen-activated protein kinase
KW - Presenilin
KW - Signal transduction
UR - http://www.scopus.com/inward/record.url?scp=19444386260&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2005.05.001
DO - 10.1016/j.bbrc.2005.05.001
M3 - Article
C2 - 15896720
AN - SCOPUS:19444386260
SN - 0006-291X
VL - 332
SP - 609
EP - 613
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -