Prion protein as trans-interacting partner for neurons is involved in neurite outgrowth and neuronal survival

Cellular Form of Prion Protein Inhibits Reelin-Mediated Shedding of Caspr from the Neuronal Cell Surface to Potentiate Caspr-Mediated Inhibition of Neurite Outgrowth

“…Cellular prion protein (PrP) is an adhesion molecule implicated in neuronal survival, neurite outgrowth (Chen et al, 2003;Santuccione et al, 2005), and synaptic function (Collinge et al, 1994). This functional feature of PrP is consistent with its association with several cell surface proteins involved in regulation of neural development, including the 67 kDa laminin receptor, the 37 kDa laminin receptor precursor protein, and the extracellular matrix glycoprotein laminin (Rieger et al, 1997;Graner et al, 2000;Gauczynski et al, 2001).…”

“…While the cellular form of PrP has been linked to neurite outgrowth and neuronal survival (Graner et al, 2000;Zanata et al, 2002;Chen et al, 2003;Santuccione et al, 2005;Lima et al, 2007), the contactin-associated protein Caspr has not been directly linked to neurite outgrowth, although its direct interaction with contactin would suggest such a function, since this GPIlinked Ig superfamily adhesion molecule promotes axonal growth (Falk et al, 2002). Caspr also interacts with the receptorlike protein tyrosine phosphatase RTPT␤ , which induces neurite outgrowth by binding to contactin (Sakurai et al, 1997).…”

“…L1-Fc (2 g/ml) (Chen et al, 1999), PrP-Fc (2 g/ml) (Chen et al, 2003), and BSA (2 g/ml) were immobilized on the polyvinylchloride surface of a 96-well microtiter plate in PBS overnight at 4°C. Nonabsorbed proteins were removed and wells were washed five times for 5 min at room temperature (RT) with PBS containing 0.05% Tween 20 (PBS-T).…”

Total Prion Protein Levels in the Cerebrospinal Fluid are Reduced in Patients with Various Neurological Disorders

“…These antioxidant properties are based on a superoxide dismutase-like activity in the octapeptidregion of the protein and seem to be involved in its neuroprotective properties by reduction of oxidative stress. Additionally, it has been shown that neuroprotection is triggered by inhibition of Bax-mediated neuronal apoptosis [11] and that PrP c is involved in the activation of several signal transduction pathways playing an important role in neuronal survival [12][13][14][15]. Recently, Parkin and colleagues demonstrated that cellular overexpression of PrP c inhibits the β-secretase cleavage of the amyloid-β protein precursor (AβPP) and reduces amyloid-β (Aβ) formation [16].…”

Pre-Clinical Changes Observed by Magnetic Resonance Imaging in a Hamster Model of Transmissible Spongiform Encephalopathy: a Potential Biomarker of Prion Infection

“…In addition, PKC has been shown to inhibit the activity of AQP4 by phosphorylating it, causing a decrease in its permeability to water [37,38]. PrP C has been implicated in cell signaling, including through both MAPK- [39,40] and PKC-dependent pathways [41]. The sequential activation of p38 MAPK has been demonstrated from 50 dpi onward in 263K scrapieinfected hamsters [42].…”