Human Amyloid beta (aa1-40) Antibody Summary
This antibody functions as an ELISA capture antibody when paired with Mouse Anti-Human APP/Protease Nexin II (Amyloid beta) Monoclonal Antibody (Catalog # MAB96182).
This product is intended for assay development on various assay platforms requiring antibody pairs. We recommend the Human Amyloid beta (aa1-40) Quantikine ELISA Kit (Catalog # DAB140B) for a complete optimized ELISA.
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Human Amyloid beta (aa1-40) ELISA Standard Curve. Recombinant Human Amyloid beta protein was serially diluted 2-fold and captured by Mouse Anti-Human Amyloid beta (aa1-40) Monoclonal Antibody (Catalog # MAB96181) coated on a Clear Polystyrene Microplate (Catalog # DY990). Mouse Anti-Human APP/Protease Nexin II (Amyloid beta) Monoclonal Antibody (Catalog # MAB96182) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998) followed by Substrate Solution (Catalog # DY999) and stopping the enzymatic reaction with Stop Solution (Catalog # DY994).
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: Amyloid beta
Amyloid Precursor Protein (APP) is a type I transmembrane protein that is ubiquitously expressed on cell surfaces. It undergoes complex proteolytic processing and is cleaved by alpha-, beta-, and gamma-Secretases to generate soluble APP alpha, soluble APP beta, and Amyloid beta (A beta) fragments of several lengths. One of these fragments, A beta 42, generated by beta- and gamma-Secretase activities, has been implicated in Alzheimer's disease. Aberrantly high levels of this peptide form and accumulate in the brains of Alzheimer's disease patients to create the senile plaques characteristic of the disease.
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