Product Name
Major prion protein (Prnp), ELISA Kit
Full Product Name
Rat Major prion protein ELISA Kit
Product Synonym Names
Major prion protein; PrP; Prnp; Prn; Prp; CD230
Product Gene Name
Prnp elisa kit
[Similar Products]
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Request for Current Manual Insert
Request Current Manual
3D Structure
ModBase 3D Structure for P13852
Detection Range
0.312-20 ng/mL
Preparation and Storage
For long term storage, please store the entire kit at -20 degree C.
Product Note
Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.
Other Notes
Small volumes of Prnp elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Searchable Terms for Prnp purchase
MBS2882431 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Major prion protein (Prnp) ELISA Kit target analytes in
biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing Prnp. The ELISA analytical biochemical technique of the MBS2882431 kit is based on Prnp antibody-Prnp antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect Prnp antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, Prnp. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).
NCBI/Uniprot data below describe general gene information for Prnp. It may not necessarily be applicable to this product.
NCBI Accession #
NP_036763.1
[Other Products]
NCBI GenBank Nucleotide #
NM_012631.2
[Other Products]
UniProt Primary Accession #
P13852
[Other Products]
UniProt Secondary Accession #
Q549H6[Other Products]
UniProt Related Accession #
P13852[Other Products]
Molecular Weight
27,804 Da
NCBI Official Full Name
major prion protein
NCBI Official Synonym Full Names
prion protein
NCBI Official Symbol
Prnp??[Similar Products]
NCBI Official Synonym Symbols
PrP; Prn
??[Similar Products]
NCBI Protein Information
major prion protein
UniProt Protein Name
Major prion protein
UniProt Synonym Protein Names
CD_antigen: CD230
Protein Family
Major prion protein
UniProt Gene Name
Prnp??[Similar Products]
UniProt Synonym Gene Names
Prn; Prp; PrP??[Similar Products]
UniProt Entry Name
PRIO_RAT
NCBI Summary for Prnp
conformational conversion of gene product prion protein (PrP) associated with Prion diseases, fatal neurodegenerative disorders in man and animal [RGD, Feb 2006]
UniProt Comments for Prnp
PRNP: 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. PrP is found in high quantity in the brain of humans and animals infected with neurodegenerative diseases known as transmissible spongiform encephalopathies or prion diseases, like: Creutzfeldt-Jakob disease (CJD), fatal familial insomnia (FFI), Gerstmann-Straussler disease (GSD), Huntington disease-like type 1 (HDL1) and kuru in humans; scrapie in sheep and goat; bovine spongiform encephalopathy (BSE) in cattle; transmissible mink encephalopathy (TME); chronic wasting disease (CWD) of mule deer and elk; feline spongiform encephalopathy (FSE) in cats and exotic ungulate encephalopathy (EUE) in nyala and greater kudu. The prion diseases illustrate three manifestations of CNS degeneration: (1) infectious (2) sporadic and (3) dominantly inherited forms. TME, CWD, BSE, FSE, EUE are all thought to occur after consumption of prion-infected foodstuffs. Defects in PRNP are the cause of Creutzfeldt-Jakob disease (CJD). CJD occurs primarily as a sporadic disorder (1 per million), while 10-15% are familial. Accidental transmission of CJD to humans appears to be iatrogenic (contaminated human growth hormone (HGH), corneal transplantation, electroencephalographic electrode implantation, etc.). Epidemiologic studies have failed to implicate the ingestion of infected annimal meat in the pathogenesis of CJD in human. The triad of microscopic features that characterize the prion diseases consists of (1) spongiform degeneration of neurons, (2) severe astrocytic gliosis that often appears to be out of proportion to the degree of nerve cell loss, and (3) amyloid plaque formation. CJD is characterized by progressive dementia and myoclonic seizures, affecting *****s in mid-life. Some patients present sleep disorders, abnormalities of high cortical function, cerebellar and corticospinal disturbances. The disease ends in death after a 3-12 months illness. Defects in PRNP are the cause of fatal familial insomnia (FFI). FFI is an autosomal dominant disorder and is characterized by neuronal degeneration limited to selected thalamic nuclei and progressive insomnia. Defects in PRNP are the cause of Gerstmann-Straussler disease (GSD). GSD is a heterogeneous disorder and was defined as a spinocerebellar ataxia with dementia and plaquelike deposits. GSD incidence is less than 2 per 100 million live births. Defects in PRNP are the cause of Huntington disease-like type 1 (HDL1). HDL1 is an autosomal dominant, early onset neurodegenerative disorder with prominent psychiatric features. Defects in PRNP are the cause of kuru (KURU). Kuru is transmitted during ritualistic cannibalism, among natives of the New Guinea highlands. Patients exhibit various movement disorders like cerebellar abnormalities, rigidity of the limbs, and clonus. Emotional lability is present, and dementia is conspicuously absent. Death usually occurs from 3 to 12 month after onset. Defects in PRNP are the cause of spongiform encephalopathy with neuropsychiatric features (SENF); an autosomal dominant presenile dementia with a rapidly progressive and protracted clinical course. The dementia was characterized clinically by frontotemporal features, including early personality changes. Some patients had memory loss, several showed aggressiveness, hyperorality and verbal stereotypy, others had parkinsonian symptoms. Belongs to the prion family. 2 isoforms of the human protein are produced by alternative initiation.
Protein type: Microtubule-binding; Membrane protein, GPI anchor
Cellular Component: anchored to plasma membrane; cell surface; cytoplasm; endoplasmic reticulum; Golgi apparatus; lipid raft; membrane; mitochondrial outer membrane; plasma membrane
Molecular Function: ATP-dependent protein binding; chaperone binding; copper ion binding; identical protein binding; lamin binding; microtubule binding; tubulin binding
Biological Process: learning and/or memory; negative regulation of activated T cell proliferation; negative regulation of apoptosis; negative regulation of interferon-gamma production; negative regulation of interleukin-17 production; negative regulation of interleukin-2 production; negative regulation of protein amino acid phosphorylation; negative regulation of T cell receptor signaling pathway; negative regulation of transcription factor activity; protein homooligomerization; regulation of protein localization; response to cadmium ion; response to copper ion; response to oxidative stress
Research Articles on Prnp
1. this study implies that lithium, the commonly used mood stabilizer, may be a promising therapeutic agent in TSE, particularly in case of the disease forms associated with accumulation of cytoPrP.
Precautions
All of MyBioSource's Products are for scientific laboratory research purposes and are not for diagnostic, therapeutics, prophylactic or in vivo use. Through your purchase, you expressly represent and warrant to MyBioSource that you will properly test and use any Products purchased from MyBioSource in accordance with industry standards. MyBioSource and its authorized distributors reserve the right to refuse to process any order where we reasonably believe that the intended use will fall outside of our acceptable guidelines.
Disclaimer
While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.
It is the responsibility of the customer to report product performance issues to MyBioSource within 30 days of receipt of the product. Please visit our Terms & Conditions page for more information.