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.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Kim MY,Park JH,Choi EJ,Park HSdoi
10.1016/j.bbrc.2005.05.001subject
Has Abstractpub_date
2005-07-01 00:00:00pages
609-13issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(05)00956-3journal_volume
332pub_type
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