Norrin; Norrie disease protein; X-linked exudative vitreoretinopathy 2 protein; NDP; EVR2

For Research Use Only. Not for use in diagnostic procedures.

For long term storage, please store the entire kit at -20 degree C.

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Small volumes of NDP 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.

MBS2882998 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Norrin (NDP) 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 NDP. The ELISA analytical biochemical technique of the MBS2882998 kit is based on NDP antibody-NDP antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect NDP antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, NDP. 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(%).

Intended Uses: This immunoassay kit allows for the in vitro quantitative determination of target antigen concentrations in serum, plasma, tissue homogenates, cell culture supernates or other biological fluids.

Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to target antigen. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific for target antigen and then avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. Then a TMB substrate solution is added to each well. Only those wells that contain target antigen, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The concentration of target antigen in the samples is then determined by comparing the O.D. of the samples to the standard curve.

15,044 Da

Norrie disease (pseudoglioma)

norrin

Norrin

EVR2??[Similar Products]

NDP_HUMAN

This gene encodes a secreted protein with a cystein-knot motif that activates the Wnt/beta-catenin pathway. The protein forms disulfide-linked oligomers in the extracellular matrix. Mutations in this gene result in Norrie disease and X-linked exudative vitreoretinopathy. [provided by RefSeq, Feb 2009]

NDP: Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction. Defects in NDP are the cause of Norrie disease (ND); also known as atrophia bulborum hereditaria or Episkopi blindness. ND is a recessive disorder characterized by very early childhood blindness due to degenerative and proliferative changes of the neuroretina. Approximately 50% of patients show some form of progressive mental disorder, often with psychotic features, and about one-third of patients develop sensorineural deafness in the second decade. In addition, some patients have more complex phenotypes, including growth failure and seizure. Defects in NDP are the cause of vitreoretinopathy exudative type 2 (EVR2). EVR2 is a disorder of the retinal vasculature characterized by an abrupt cessation of growth of peripheral capillaries, leading to an avascular peripheral retina. This may lead to compensatory retinal neovascularization, which is thought to be induced by hypoxia from the initial avascular insult. New vessels are prone to leakage and rupture causing exudates and bleeding, followed by scarring, retinal detachment and blindness. Clinical features can be highly variable, even within the same family. Patients with mild forms of the disease are asymptomatic, and their only disease related abnormality is an arc of avascular retina in the extreme temporal periphery.

Protein type: Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: Xp11.4

Cellular Component: cell surface; extracellular matrix; extracellular space

Molecular Function: cytokine activity; frizzled binding; growth factor activity; protein binding; protein homodimerization activity

Biological Process: cell proliferation; cell-cell signaling; nervous system development; placenta development; positive regulation of transcription factor activity; positive regulation of transcription, DNA-dependent; sensory perception of sound; signal transduction; vacuole organization and biogenesis; visual perception; Wnt receptor signaling pathway; Wnt receptor signaling pathway through beta-catenin

Disease: Exudative Vitreoretinopathy 2, X-linked; Norrie Disease

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