AB5078P
Anti-Beta-Amyloid 1-42 Antibody
Chemicon®, from rabbit
Synonym(s):
Anti-AAA, Anti-ABETA, Anti-ABPP, Anti-AD1, Anti-APPI, Anti-CTFgamma, Anti-CVAP, Anti-PN-II, Anti-PN2, Anti-alpha-sAPP, Anti-preA4
Sign Into View Organizational & Contract Pricing
All Photos(3)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
biological source
rabbit
Quality Level
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
chicken, mouse, human
manufacturer/tradename
Chemicon®
technique(s)
ELISA: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... APP(351)
General description
The cerebral and vascular plaques associated with Alzheimer′s disease (AD) are mainly composed of amyloid beta peptides (Ab). Ab is derived from cleavage of the amyloid precursor protein (APP) and varies in length from 39 to 43 amino acids. Ab [1-40], Ab [1-42], and Ab [1-43] peptides result from cleavage of APP after residues 40, 42, and 43, respectively. The cleavage takes place by gamma-secretase during the last APP processing step. Ab [1-40], [1-42] and [1-43] peptides are major constituents of the plaques and tangles that occur in AD. Ab antibodies and peptides have been developed as tools for elucidating the biology of AD.
Specificity
Recognizes beta-amyloid 1-42. Antibody does not show appreciable reactivity with beta amyloid 1-40 as detected by ELISA.
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.
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.
Immunogen
A six amino acid peptide sequence from the C-terminal of human beta-amyloid 1-42.
Epitope: C-terminus
Application
Anti-Beta-Amyloid 1-42 Antibody is an antibody against Beta-Amyloid 1-42 for use in ELISA, IH, IH(P) & WB.
Immunohistochemistry (Paraffin) Analysis:
Western Blot:
1-10 µg/mL of a previous lot was used. (Chemiluminescence technique).
ELISA:
1:10,000-1:100,000 of a previous lot was used using 50-100 ng immunogen peptide/well.
Optimal working dilutions must be determined by the end user.
Western Blot:
1-10 µg/mL of a previous lot was used. (Chemiluminescence technique).
ELISA:
1:10,000-1:100,000 of a previous lot was used using 50-100 ng immunogen peptide/well.
Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
Quality
Routinely evaluated by immunohistochemistry (paraffin) on Alzheimer’s Disease-Brain.
Immunohistochemistry (Paraffin) Analysis:
Beta-Amyloid (cat. # AB5078P) staining on Alzheimer’s Disease-Brain. Tissue pretreated with Citrate, pH 6.0. The antibody was diluted to 1:35, using IHC-Select Detection with HRP-DAB. Immunoreactivity is seen as staining on plaque deposits (brown) or as cerebral vascular amyloid deposition in the walls of blood vessels (brown).
Immunohistochemistry (Paraffin) Analysis:
Beta-Amyloid (cat. # AB5078P) staining on Alzheimer’s Disease-Brain. Tissue pretreated with Citrate, pH 6.0. The antibody was diluted to 1:35, using IHC-Select Detection with HRP-DAB. Immunoreactivity is seen as staining on plaque deposits (brown) or as cerebral vascular amyloid deposition in the walls of blood vessels (brown).
Physical form
ImmunoAffinity Purified
Purified rabbit polyclonal in liquid buffer containing PBS with 0.1% BSA.
Storage and Stability
Stable for 1 year at -20ºC from date of receipt.
Analysis Note
Control
Alzheimer′s disease brain tissue, whole tissue extracts from mouse brain. C03-801.
Alzheimer′s disease brain tissue, whole tissue extracts from mouse brain. C03-801.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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.
Not finding the right product?
Try our Product Selector Tool.
Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
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’.
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
Customers Also Viewed
Neuroglobin attenuates beta-amyloid neurotoxicity in vitro and transgenic Alzheimer phenotype in vivo.
Khan, AA; Mao, XO; Banwait, S; Jin, K; Greenberg, DA
Proceedings of the National Academy of Sciences of the USA null
Accumulation of intraneuronal ?-amyloid 42 peptides is associated with early changes in microtubule-associated protein 2 in neurites and synapses.
Takahashi, RH; Capetillo-Zarate, E; Lin, MT; Milner, TA; Gouras, GK
Testing null
Nicotinic receptor agonists and antagonists increase sAPPalpha secretion and decrease Abeta levels in vitro.
M Mousavi,E Hellstrom-Lindahl
Neurochemistry International null
Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid deposition.
M Dumont, DJ Ho, NY Calingasan, H Xu, G Gibson, MF Beal
Free radical biology & medicine null
N-iminoethyl-L-lysine improves memory and reduces amyloid pathology in a transgenic mouse model of amyloid deposition.
M Dumont, E Wille, NY Calingasan, C Nathan, M Flint Beal, MT Lin
Neurochemistry International null
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service