Anti-PRNP monoclonal antibody, clone 2F6/H7

Name: Anti-PRNP monoclonal antibody, clone 2F6/H7
SKU: DCABH-8470
Rating: 5 (1 reviews)

Mouse anti-Bovine PRNP monoclonal antibody for ELISA, WB

COA

SDS

Datasheet

Additional Formats Available

Summary

Specifications

Antibody Isotype

IgG1

Clone

2F6/H7

Species Reactivity

Bovine

Immunogen

Recombinant bovine prion protein. Immunization was performed according to the protocol described by Hofmann, J. et al.

Conjugate

Unconjugated

Target

Alternative Names

PRNP; prion protein; major prion protein; prion protein PrP; prion protein precursor PrP; major scrapie-associated fibril protein 1; prion protein (p27-30) (Creutzfeldt-Jakob disease, Gerstmann-Strausler-Scheinker syndrome, fatal familial insomnia); PrP;

Entrez Gene ID

281427

UniProt ID

F7VJQ2

Product Background

Antigen Description

The function of PrP is still under debate. 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 (By similarity). Isoform 2 may act as a growth suppressor by arresting the cell cycle at the G0/G1 phase. Soluble oligomers are toxic to cultured neuroblastoma cells and induce apoptosis (in vitro).

Pathway

Axon guidance, organism-specific biosystem; Developmental Biology, organism-specific biosystem; NCAM signaling for neurite out-growth, organism-specific biosystem; NCAM1 interactions, organism-specific biosystem; Prion diseases, organism-specific biosystem; Prion diseases, conserved biosystem;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Prion protein gene polymorphisms in Turkish native goat breeds

JOURNAL OF GENETICS

Authors: Meydan, Hasan; Pehlivan, Erkan; Ozkan, Mustafa Muhip; Yildiz, Mehmet Ali; Goldmann, Wilfred

Abstract

Susceptibility to 'scrapie' disease in goats is influenced by polymorphisms of the prion protein (PRNP) gene. The aim of this study was to identify PRNP gene polymorphisms in a total of 356 scrapie disease-free goats from 10 Turkish native breeds. Eighteen single-nucleotide polymorphisms were detected in the caprine PRNP open-reading frame. Ten previously described amino acid substitutions (I142M, H143R, N146S, N146D, R151H, R154H, P168Q, R211Q, Q222K and P240S) and two novel dimorphisms (G134E and Q163P) were identified. The strongest association between caprine PRNP and relative resistance to scrapie disease has been reported previously for polymorphisms at codons 146 (S /D) and 222 (K). In the present study, these three PrP variants were relatively rare with 6.3%. This is the first report on PRNP gene variation in Turkish native goat breeds and our knowledge of these polymorphisms will assist goat breeding programmes to reduce the risk of scrapie.

Impairment of cerebellar long-term depression and GABAergic transmission in prion protein deficient mice ectopically expressing PrPLP/Dpl

SCIENTIFIC REPORTS

Authors: Kishimoto, Yasushi; Hirono, Moritoshi; Atarashi, Ryuichiro; Sakaguchi, Suehiro; Yoshioka, Tohru; Katamine, Shigeru; Kirino, Yutaka

Abstract

Prion protein (PrPC) knockout mice, named as the "Ngsk" strain (Ngsk Prnp(0/0) mice), show late-onset cerebellar Purkinje cell (PC) degeneration because of ectopic overexpression of PrPC-like protein (PrPLP/Dpl). Our previous study indicated that the mutant mice also exhibited alterations in cerebellum-dependent delay eyeblink conditioning, even at a young age (16 weeks of age) when neurological changes had not occurred. Thus, this electrophysiological study was designed to examine the synaptic function of the cerebellar cortex in juvenile Ngsk Prnp(0/0) mice. We showed that Ngsk Prnp(0/0) mice exhibited normal paired-pulse facilitation but impaired long-term depression of excitatory synaptic transmission at synapses between parallel fibres and PCs. GABA(A)-mediated inhibitory postsynaptic currents recorded from PCs were also weakened in Ngsk Prnp(0/0) mice. Furthermore, we confirmed that Ngsk Prnp(0/0) mice (7-8-week-old) exhibited abnormalities in delay eyeblink conditioning. Our findings suggest that these alterations in both excitatory and inhibitory synaptic transmission to PCs caused deficits in delay eyeblink conditioning of Ngsk Prnp(0/0) mice. Therefore, the Ngsk Prnp(0/0) mouse model can contribute to study underlying mechanisms for impairments of synaptic transmission and neural plasticity, and cognitive deficits in the central nervous system.