|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||27661 Da|
|Other Names||Major prion protein, PrP, ASCR, PrP27-30, PrP33-35C, CD230, PRNP, ALTPRP, PRIP, PRP|
|Target/Specificity||A synthetic peptide corresponding to residues near the C-terminus of human Prp was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Prion Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||ALTPRP, PRIP, PRP|
|Function||May play a role in neuronal development and synaptic plasticity. May be required for neuronal myelin sheath maintenance. May play a role in iron uptake and iron homeostasis. Soluble oligomers are toxic to cultured neuroblastoma cells and induce apoptosis (in vitro). Association with GPC1 (via its heparan sulfate chains) targets PRNP to lipid rafts. Also provides Cu(2+) or ZN(2+) for the ascorbate-mediated GPC1 deaminase degradation of its heparan sulfate side chains (By similarity).|
|Cellular Location||Cell membrane; Lipid-anchor, GPI-anchor. Golgi apparatus. Note=Targeted to lipid rafts via association with the heparan sulfate chains of GPC1. Colocates, in the presence of CU(2+), to vesicles in para- and perinuclear regions, where both proteins undergo internalization. Heparin displaces PRNP from lipid rafts and promotes endocytosis|
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Provided below are standard protocols that you may find useful for product applications.
Prion diseases are transmissible neurodegenerative disorders which affect a range of mammalian species. In humans they can be inherited and sporadic as well as acquired by exposure to human prions. Prions appear to be composed principally of a conformational isomer of host-encoded prion protein and propagate by recruitment of cellular prion protein (1). The function of the cellular prion protein (PrP) is still poorly understood. It has been proposed that one unprecedented role for PrP is against Bax-mediated neuronal apoptosis. It has been shown that PrP potently inhibits Bax-induced cell death in human primary neurons (2). An impaired synaptic inhibition may be involved in the epileptiform activity seen in Creutzfeldt-Jakob and other neurodegenerative diseases and it is believed that loss of function of PrP may contribute to the early synaptic loss and neuronal degeneration seen in these diseases (3).
1. Collinge J, Hum Mol Genet 6(10):1699-705, 1997
2. Bounhar Y, et al. J Biol Chem 276(42):39145-9, 2001
3. Collinge J, et al. Nature 370(6487):295-7, 1994
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