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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Clone:
polyclonal
Species reactivity:
human, mouse
Application:
ELISA, IHC, WB
Citations:
31
Product Name
Anti-Amyloid Antibody, β 1-40/42, serum, Chemicon®
biological source
rabbit
Quality Level
antibody form
serum
antibody product type
primary antibodies
clone
polyclonal
species reactivity
human, mouse
manufacturer/tradename
Chemicon®
technique(s)
ELISA: suitable, immunohistochemistry: suitable, western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... APP(351)
Immunogen
A synthetic beta-amyloid peptide 1-40 conjugated to BSA.
Application
Anti-Amyloid Antibody, β 1-40/42 is an antibody against Amyloid for use in ELISA, IH & WB.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
Western blot: 1:1,000-1:5,000 (Chemiluminescence technique)
Immunohistochemistry: 1:100 using formalin or paraformaldehyde fixed Alzheimer′s brain tissue.
ELISA: 1:10,000-1:100,000 (50-100 ng immunogen peptide /well).
Immunoge control peptide is Catalog number AG365.
Optimal working dilutions must be determined by the end user.
Immunohistochemistry: 1:100 using formalin or paraformaldehyde fixed Alzheimer′s brain tissue.
ELISA: 1:10,000-1:100,000 (50-100 ng immunogen peptide /well).
Immunoge control peptide is Catalog number AG365.
Optimal working dilutions must be determined by the end user.
Biochem/physiol Actions
Recognizes beta-amyloid 1-40/42. One of the most important and initial steps which causes loss of memory and cognition in Alzheimer′s Disease (AD) involves proteolytic cleavage of amyloid precursor protein (APP, chromosome 21) releasing short 40, 42 & 43 amino acid peptides (beta amyloid 1-40, 1-42 and 1-43). Polymerization of beta-amyloid and subsequent neuronal deposit (amyloid) leads to the degeneration of neurons involved in memory and cognition. The immunogen peptide shows homology with beta-amyloid 1-28 and beta-amyloid 12-28. No cross reactivity is observed with CGRP.
Physical form
Rabbit Serum. Liquid and 0.1% sodium azide.
Unpurified
Preparation Note
Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Analysis Note
Control
Alzheimer′s disease brain tissue, whole tissue extracts from mouse brain
Alzheimer′s disease brain tissue, whole tissue extracts from mouse brain
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Replaces: AB5408
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Related Content
Alzheimer’s Disease: Amyloid Cascade and Beyond Product Focus
Pedram Honarpisheh et al.
International journal of molecular sciences, 21(5) (2020-03-07)
Amyloid plaques in Alzheimer's disease (AD) are associated with inflammation. Recent studies demonstrated the involvement of the gut in cerebral amyloid-beta (Aβ) pathogenesis; however, the mechanisms are still not well understood. We hypothesize that the gut bears the Aβ burden
Tomoharu Kuboyama et al.
Frontiers in pharmacology, 8, 805-805 (2017-12-01)
Memory impairments in Alzheimer's disease (AD) occur due to degenerated axons and disrupted neural networks. Since only limited recovery is possible after the destruction of neural networks, preventing axonal degeneration during the early stages of disease progression is necessary to
Synergistic effects of high fat feeding and apolipoprotein E deletion on enterocytic amyloid-beta abundance.
Galloway, S; Pallebage-Gamarallage, MM; Takechi, R; Jian, L; Johnsen, RD; Dhaliwal, SS; Mamo, JC
Lipids in Health and Disease null
Global Trade Item Number
| SKU | GTIN |
|---|---|
| AB5076 | 04053252329425 |