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Identification and characterisation of the novel amyloid-beta peptide-induced protein p17.

Authors: Nehar, S  Mishra, M  Heese, K 
Citation: Nehar S, etal., FEBS Lett. 2009 Oct 6;583(19):3247-53. doi: 10.1016/j.febslet.2009.09.018. Epub 2009 Sep 13.
Pubmed: (View Article at PubMed) PMID:19755123
DOI: Full-text: DOI:10.1016/j.febslet.2009.09.018

Amyloid-beta peptide (Abeta) achieves neurodegeneration through unknown mechanisms. To elucidate some of these mechanisms, we conducted a cDNA subtraction analysis of Abeta-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 Abeta-mediated pro-apoptotic pathways in AD.


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CRRD Object Information
CRRD ID: 8553945
Created: 2014-05-08
Species: All species
Last Modified: 2014-05-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.