| First Author | Gavín R | Year | 2005 |
| Journal | FEBS Lett | Volume | 579 |
| Issue | 19 | Pages | 4099-106 |
| PubMed ID | 16023105 | Mgi Jnum | J:346484 |
| Mgi Id | MGI:7616530 | Doi | 10.1016/j.febslet.2005.06.037 |
| Citation | Gavin R, et al. (2005) PrP(106-126) activates neuronal intracellular kinases and Egr1 synthesis through activation of NADPH-oxidase independently of PrPc. FEBS Lett 579(19):4099-106 |
| abstractText | Prion diseases are characterised by severe neural lesions linked to the presence of an abnormal protease-resistant isoform of cellular prion protein (PrPc). The peptide PrP(106-126) is widely used as a model of neurotoxicity in prion diseases. Here, we examine in detail the intracellular signalling cascades induced by PrP(106-126) in cortical neurons and the participation of PrPc. We show that PrP(106-126) induces the activation of subsets of intracellular kinases (e.g., ERK1/2), early growth response 1 synthesis and induces caspase-3 activity, all of which are mediated by nicotinamide adenine dinucleotide phosphate hydrogen-oxidase activity and oxidative stress. However, cells lacking PrPc are similarly affected after peptide exposure, and this questions the involvement of PrPc in these effects. |
