ELISA/assay

Human Agrin ELISA Kit

MBS721753

48-Strip-Wells-(Competitive)

440 USD

ELISA Kit

Human Agrin ELISA Kit

[Agrin]

[agrin, partial; Agrin; agrin; agrin proteoglycan; agrin]

[Agrin]

[AGRN; AGRN; CMSPPD; AGRIN; C90; C22]

AGRIN_HUMAN

Human

This assay has high sensitivity and excellent specificity for detection of AGR-Ab. No significant cross-reactivity or interference between AGR-Ab and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between AGR-Ab and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma, Cell Culture Supernatants, Body Fluid And Tissue Homogenate. Assay Type: Quantitative Competitive. Sensitivity: 1.0 ng/mL.

Neurobiology

Intended Uses: This AGR-Ab ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human AGR-Ab. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: AGR-Ab ELISA kit applies the competitive enzyme immunoassay technique utilizing a AGR antigen and an AGR-Ab-HRP conjugate. The assay sample and buffer are incubated together with AGR-Ab-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the AGR-Ab concentration since AGR-Ab from samples and AGR-Ab-HRP conjugate compete for the AGR antigen binding site. Since the number of sites is limited, as more sites are occupied by AGR-Ab from the sample, fewer sites are left to bind AGR-Ab-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The AGR-Ab concentration in each sample is interpolated from this standard curve.

255738

AAB23327.1

216,733 Da

A Tetrasaccharide Linker Sequence Is Required For GAG Synthesis Pathway (645305); Axon Guidance Pathway (105688); Chondroitin Sulfate/dermatan Sulfate Metabolism Pathway (645308); Developmental Biology Pathway (477129); Disease Pathway (530764); Diseases Associated With Visual Transduction Pathway (771581); ECM Proteoglycans Pathway (833812); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479); Extracellular Matrix Organization Pathway (576262)

This gene encodes one of several proteins that are critical in the development of the neuromuscular junction (NMJ), as identified in mouse knock-out studies. The encoded protein contains several laminin G, Kazal type serine protease inhibitor, and epidermal growth factor domains. Additional post-translational modifications occur to add glycosaminoglycans and disulfide bonds. In one family with congenital myasthenic syndrome affecting limb-girdle muscles, a mutation in this gene was found. [provided by RefSeq, Aug 2011]

AGRN: Plays a central role in the formation and the maintenance of the neuromuscular junction (NMJ), the synapse between motor neuron and skeletal muscle. Ligand of the MUSK signaling complex that directly binds LRP4 in this complex and induces the phosphorylation of MUSK, the kinase of the complex. The activation of MUSK in myotubes induces the formation of NMJ by regulating different processes including the transcription of specific genes and the clustering of AChR in the postsynaptic membrane. Defects in AGRN are a cause of myasthenia, limb-girdle, familial (LGM). A congenital myasthenic syndrome characterized by a typical limb girdle pattern of muscle weakness with small, simplified neuromuscular junctions but normal acetylcholine receptor and acetylcholinesterase function. Protein type: Cell development/differentiation; Cell adhesion; Secreted, signal peptide; Secreted; Extracellular matrix. Chromosomal Location of Human Ortholog: 1p36.33. Cellular Component: extracellular matrix; extracellular space; lysosomal lumen; cell surface; Golgi lumen; cytoplasm; plasma membrane; integral to membrane; extracellular region; basal lamina; synapse; cell junction. Molecular Function: heparan sulfate proteoglycan binding; protein binding; structural constituent of cytoskeleton; acetylcholine receptor regulator activity; laminin binding; calcium ion binding; sialic acid binding. Biological Process: positive regulation of filopodium formation; clustering of voltage-gated sodium channels; phototransduction, visible light; axon guidance; extracellular matrix organization and biogenesis; acetylcholine receptor signaling, muscarinic pathway; glycosaminoglycan metabolic process; neurotransmitter receptor metabolic process; pathogenesis; positive regulation of synaptic growth at neuromuscular junction; signal transduction; receptor clustering; chondroitin sulfate metabolic process; glycosaminoglycan biosynthetic process; glycosaminoglycan catabolic process; plasma membrane organization and biogenesis; positive regulation of neuron apoptosis; carbohydrate metabolic process; synapse organization and biogenesis; positive regulation of transcription from RNA polymerase II promoter; regulation of receptor activity; retinoid metabolic process; neuromuscular junction development. Disease: Myasthenic Syndrome, Congenital, With Pre- And Postsynaptic Defects

48-Strip-Wells-(Competitive)

440 USD

48-Strip-Wells-(Sandwich)

440

96-Strip-Wells-(Competitive)

640

96-Strip-Wells-(Sandwich)

640

5x96-Strip-Wells-(Competitive)

2895

5x96-Strip-Wells-(Sandwich)

2895

10x96-Strip-Wells-(Competitive)

5415

10x96-Strip-Wells-(Sandwich)

5415