PrP (106-126) is a peptide corresponding to the prion protein (PrP) amyloidogenic region, and its biochemical properties resemble the infectious form of prion protein.

PrP (106-126) (100 μM) induces mTOR phosphorylation over time in N2a cells. PrP (106-126)-treated cells show significantly increased ROS production in comparison with that of PBS-treated control cells. Knockdown of PRAS40 enhances PrP (106-126)-induced apoptosis. PRAS40 alleviates PrP (106-126)-induced neuronal apoptosis via mTOR-AKT activation. PrP (106-126) interacts selectively with porcine brain endothelial cells (PBEC) via their luminal side, and causes cumulative cell death, as shown by lactate dehydrogenase release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction, Caspase 3 induction and direct cell counting. In addition, PrP (106-126), but not its corresponding scrambled peptide, produces a 50% reduction of the trans-endothelial electrical resistance, while the PBEC maintained confluency.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Yang W, et al. PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling. CNS Neurosci Ther. 2017 May;23(5):416-427.  [Content Brief]

  . Cooper I, et al. Interactions of the prion peptide (PrP 106-126) with brain capillary endothelial cells: coordinated cell killing and remodeling of intercellular junctions. J Neurochem. 2011 Feb;116(4):467-75.  [Content Brief]