Journal
FEBS LETTERS
Volume 583, Issue 19, Pages 3247-3253Publisher
WILEY
DOI: 10.1016/j.febslet.2009.09.018
Keywords
Amyloid; Alzheimer's disease; TrkB; BDNF; Neurotrophin
Funding
- A*STAR [BMRC/04/1/22/19/360]
Ask authors/readers for more resources
Amyloid-beta peptide (Ab) achieves neurodegeneration through unknown mechanisms. To elucidate some of these mechanisms, we conducted a cDNA subtraction analysis of Ab-mediated neurotoxicity in neuronal cells and observed an up-regulation of the novel gene p17. The p17 protein was also found elevated in Alzheimer's disease (AD) mouse model. Here, we characterised p17 primarily in cell lines with respect to its localisation, function and physiological expression. We discovered that p17 acts downstream of protein kinase C and inhibits the tyrosine receptor kinase B-brain-derived neurotrophic factor (TrkB-BDNF) pathway. It impedes survival factors and enhances amyloid precursor protein expression thus suggesting its involvement in the Ab-mediated pro-apoptotic pathways in AD. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available