Amyloid beta (1-17) Mouse Monoclonal Antibody [Clone ID: DE2B4]

Specifications

Product Data
Clone Name	DE2B4
Applications	ELISA, IHC, IP
Recommend Dilution	ELISA. Immunoprecipitation. Immunohistochemistry on Paraffin Sections: This product requires protein digestion pre-treatment of paraffin sections using formic acid for 2-3 minutes. Recommended Positive Control: Alzheimers disease brain.
Reactivity	Human
Host	Mouse
Clonality	Monoclonal
Immunogen	Synthetic peptide consisting of residues 1-17 of the Amyloid beta protein.
Specificity	This antibody recognises the beta Amyloid peptide, which is the major protein component of the Amyloid cores in neuritic plaques. In Immunohistology the antibody detects extracellular Amyloid beta with senile plaques and vessel amyloid in Alzheimers disease brain.
Isotype	IgG1
Formulation	PBS State: Purified State: Liquid purified IgG fraction from tissue culture supernatant Preservative: 0.09% Sodium Azide
Concentration	lot specific
Purification	Affinity Chromatography on Protein G
Conjugation	Unconjugated
Storage Condition	Store undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing.
Background	Amyloid beta precursor protein gene (ABPP) encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Multiple transcript variants encoding several different isoforms have been found for this gene. Isoform APP695 is the predominant form in neuronal tissue, isoform APP751 and isoform APP770 are widely expressed in nonneuronal cells. Isoform APP751 is the most abundant form in T lymphocytes. ABPP is expressed in all fetal tissues examined with the highest levels in brain, kidney, heart and spleen with weak expression observed in liver; ABPP is induced during neuronal differentiation. In the adult brain, highest expression of ABPP gene is found in the frontal lobe of the cortex and in the anterior perisylvian cortex opercular gyri; moderate expression in the cerebellar cortex, the posterior perisylvian cortex opercular gyri and the temporal associated cortex. Weak expression is found in the striate, extra striate and motor cortices. Mutations in ABPP have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy).
Reference Data

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