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PMID:15896720

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Citation

Kim, MY, Park, JH, Choi, EJ and Park, HS (2005) Presenilin acts as a positive regulator of basal level activity of ERK through the Raf-MEK1 signaling pathway. Biochem. Biophys. Res. Commun. 332:609-13

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.

Links

PubMed Online version:10.1016/j.bbrc.2005.05.001

Keywords

Animals; Basal Metabolism/physiology; Cells, Cultured; Extracellular Signal-Regulated MAP Kinases/metabolism; Fibroblasts/metabolism; Gene Expression Regulation/physiology; MAP Kinase Kinase 1/metabolism; Membrane Proteins/metabolism; Mice; Mitogen-Activated Protein Kinases/metabolism; Presenilin-1; Signal Transduction/physiology; raf Kinases/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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