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AB5078P

Sigma-Aldrich

Anti-Beta-Amyloid 1-42 Antibody

Chemicon®, from rabbit

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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
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)

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This Item
MABN12MABN11ABN240
vibrant-m

AB5078P

Anti-Beta-Amyloid 1-42 Antibody

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

antibody form

affinity purified immunoglobulin

antibody form

purified immunoglobulin

antibody form

purified antibody

antibody form

affinity isolated antibody

species reactivity

chicken, mouse, human

species reactivity

human, mouse

species reactivity

human, mouse

species reactivity

human

Gene Information

human ... APP(351)

Gene Information

human ... APP(351)

Gene Information

human ... APP(351)

Gene Information

human ... APP(351)

NCBI accession no.

NM_000484.2

NCBI accession no.

NP_000475

NCBI accession no.

NP_000475

NCBI accession no.

NP_001129601

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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.

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.
Research Category
Neuroscience
Research Sub Category
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).

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.

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.

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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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
Chronic thrombin exposure results in an increase in apolipoprotein-E levels.
Mhatre, M; Hensley, K; Nguyen, A; Grammas, P
Journal of Neuroscience Research null
Ramon Velazquez et al.
Molecular neurodegeneration, 11(1), 52-52 (2016-07-15)
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder worldwide. Clinically, AD is characterized by impairments of memory and cognitive functions. Accumulation of amyloid-β (Aβ) and neurofibrillary tangles are the prominent neuropathologies in patients with AD. Strong evidence indicates that
Constantinos D Paspalas et al.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 14(5), 680-691 (2017-12-16)
An animal model of late-onset Alzheimer's disease is needed to research what causes degeneration in the absence of dominant genetic insults and why the association cortex is particularly vulnerable to degeneration. We studied the progression of tau and amyloid cortical
Matthew M Harper et al.
Investigative ophthalmology & visual science, 60(7), 2716-2725 (2019-06-28)
Traumatic brain injury (TBI) is a risk factor for developing chronic neurodegenerative conditions including Alzheimer's disease (AD). The purpose of this study was to examine chronic effects of blast TBI on retinal ganglion cells (RGC), optic nerve, and brain amyloid

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