#10027 Anti-Human Amyloidβ (11-28) (12B2) Mouse IgG MoAb

References (0)
FAQ (0)
Related Materials (0)
Related Products (0)

References (0)
FAQ (0)
Related Materials (0)
Related Products (0)

Intended Use：: Research reagents

Application：: WB, IP, IHC

Package Size1：: 50 μg

Package Size2：: 5 μg

Note on Application Abbreviations: WB:Western Blotting; IP:Immunoprecipitation; IHC:Immunohistochemistry

※ The product indicated as "Research reagents" in the column Intended Use cannot be used
　 for diagnostic nor any medical purpose.
※ The datasheet listed on this page is sample only. Please refer to the datasheet
　 enclosed in the product purchased before use.

Product Overview

Product Code	10027
Product Name	Anti-Human Amyloidβ (11-28) (12B2) Mouse IgG MoAb
Intended Use	Research reagents
Application	WB, IP, IHC
Species	Human
Immunizing antigen	Synthetic peptide of a part of human Amyloidβ, (11-28)
Source	Mouse-Mouse hybridoma
Clone Name	12B2
Subclass	IgG1
Purification Method	Affinity purified with antigen peptide
Specificity	Reacts with human Amyloidβ (1-40), (1-42) and (1-43)
Package Form	Lyophilized product from PBS containing 1 % BSA and 0.05 % NaN3
Storage Condition	2 - 8℃
Poisonous and Deleterious Substances	Applicable
Cartagena	Not Applicable
Package Size 1	50 μg
Package Size 2	5 μg
Remarks1	The commercial use of products without our permission is prohibited. Please make sure to contact us and obtain permission.

Product Description

Alzheimer's disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein component of these plaques is beta amyloid (Aβ) peptide, a 40 to 43 amino acid peptide cleaved from amyloid precursor protein by β-secretase and γ-secretase. Increased release of Aβ42 or Aβ43, both of which exibit a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations, ApoE alleles or may involve other undiscovered factors. Many researchers theorize that it is this increased release of Aβ42/Aβ43 which leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals. It is also reported that a distinct Aβpeptide, AβN3pE, is deposited in senile plaques in a dominant and differential manner as compared with the standard Aβpeptide.