Amyloid-β Antibody – MCA-AB9

Encor Mouse Monoclonal to Amyloid Aβ, A-beta: APP

Alzheimer’s disease (AD) is a serious and common age related dementia which is characterized by the formation of senile plaques and neurofibrillary tangles. Senile plaques are extracellular accumulations of insoluble proteins found in cortical regions. A major component of senile plaques is β-amyloid, a.k.a. Aβ, a peptide predominantly of 42 or 40 amino acids.
The Aβ peptide is derived from a section of the membrane spanning domain and the immediate extracellular region of a much larger protein called the amyloid precursor protein (APP). This is an abundant protein of poorly understood function.

The Aβ peptides are generated by the activity of proteases called secretases, specifically the β and γ secretases. Certain mutations in the APP gene are associated with familial forms of AD, as are mutations in the genes encoding proteins forming the secretase enzymes, in line with the hypothesis that Aβ accumulation is central to the AD disease process.

Our antibody recognizes amino acids 1-16 of the Aβ peptide and works well on western blots, on formalin fixed sections and as a capture reagent in ELISA. It was originally developed in the Mayo Clinic in Jacksonville in the laboratory of Dr. Todd Golde.

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HGNC name(s) : APBA

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Host : Mouse

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Clonality : Monoclonal

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ID : EnCor Biotechnology Amyloid-β AB9

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Reactivity : Human | Horse | Cow | Pig | Chicken | Rat | Mouse

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Isotype : IgG2a

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Conjugation : none

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Immunogen : Amino acids 1-42

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Mass of detected protein : 5 kDa

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Uniprot ID : Q99767

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KGNC name : APBA

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RRID # : AB_2572226

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Purification : Affinity purified at 1 mg/mL

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Storage : Shipped on ice. Store at 4°C. For long term storage, leave frozen at -20°C. Avoid freeze / thaw cycles.

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Validated applications : WB | IF/ICC | IHC

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Suggested Dilutions:

WB: 1:1 000-1:2 000
IF/IHC: 1:1 000

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Datasheet

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Link to on EnCor’s website

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References :

1. Levites, Y., Das, P., Price, R. W., Rochette, M. J., Kostura, L. A., McGowan, E. M., Murphy, M. P., and Golde, T. E. (2006) Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse model, The Journal of clinical investigation 116, 193-201.

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