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Decrease in NF-kappaB, AP-1 and SP-1 activities in neuronal cells expressing presenilin 2
Hong Nga Nguyen1, Sun Young Lee, Dae Youn Hwang
1College of Pharmacy, Chungbuk National University, Chungbuk 361-763, Korea.
Neuroreport
|April 29, 2005
Summary
Presenilin 2 may cause neuronal cell death by reducing the activity of antiapoptotic transcription factors like NF-kappaB, AP-1, and SP-1. This effect was observed in transfected cells and mouse brain cells, particularly those with mutant presenilin 2.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Presenilin 2 (PSEN2) is a component of the gamma-secretase complex.
- Dysregulation of PSEN2 is linked to neurodegenerative diseases.
- Transcription factors like NF-kappaB, AP-1, and SP-1 play roles in cell survival.
Purpose of the Study:
- To investigate the effect of presenilin 2 on the activity of key transcription factors.
- To determine if presenilin 2 influences apoptotic and antiapoptotic pathways in neuronal cells.
Main Methods:
- Transfection of PC12 cells with presenilin 2.
- Analysis of transcription factor activity (NF-kappaB, AP-1, SP-1) under basal and apoptotic conditions.
- Examination of presenilin 2 expression and transcription factor activity in mouse brain cells.
Main Results:
- Presenilin 2 transfection led to decreased activity of NF-kappaB, AP-1, and SP-1 in PC12 cells.
- Reduced transcription factor activity was observed even without apoptotic stimulation.
- Similar decreases in transcription factor activity were found in mouse brain cells expressing presenilin 2, especially mutant forms.
Conclusions:
- Presenilin 2 may contribute to neuronal cell death.
- The mechanism involves the modulation of antiapoptotic transcription factors.
- Presenilin 2's role in altering transcription factor activity suggests a link to neurodegeneration.