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MilliporeSigma

MAB348

Sigma-Aldrich

Anti-Beta (β)-Amyloid antibody

CHEMICON®, mouse monoclonal, 22C11

Synonym(s):

APP, Anti - APP A4, Anti-amyloid precursor protein A4

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

Key Documents

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Product Name

Anti-APP A4 Antibody, a.a. 66-81 of APP {NT}, clone 22C11, clone 22C11, Chemicon®, from mouse

biological source

mouse

Quality Level

100

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

22C11, monoclonal

species reactivity

rat, fish, human, mouse, canine, pig, monkey

manufacturer/tradename

Chemicon®

technique(s)

immunofluorescence: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable

isotype

IgG1

NCBI accession no.

NM_000484.2
NM_201413.1
NM_201414.1

UniProt accession no.

P05067

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... APP(351)

General description

110/120/130 kDa
The β/A4 amyloid precursor protein (APP) is a transmembrane glycoprotein and exists in three isoforms. This protein is composed of a single-pass transmembrane domain, a large extracellular N-terminal domain, and a short cytoplasmic C-terminal tail. The APP gene is located on the human chromosome at 21q21.3-q22.

Immunogen

Epitope: a.a. 66-81 of APP {N-terminus}
Purified recombinant Alzheimer precursor A4 (pre A4695) fusion protein.

Application

Anti-APP A4 Antibody, a.a. 66-81 of APP , clone 22C11 has been used in immunohistochemistry and immunoblotting(1:1000).

Biochem/physiol Actions

Anti-APP A4 Antibody reacts with pre-A4 and recognizes amino acids 66-81 of the N-terminus on the pre-A4 molecule (Hilbich et al., 1993). 22C11 recognizes all three isoforms of APP, immature ~110kDa, sAPP ~120kDa, and mature ~130kDa (Hoffmann et al., 2000). The Anti-APP A4 antibody is known to cross-react with APLP2 (Slunt, 1994).
The β/A4 amyloid precursor protein (APP) undergoes proteolytic cleavage and produces β/A4 peptide. The extracellular deposition of this peptide is observed in brain cortical parenchyma and cerebro-meningeal blood vessels which marks the pathological condition of Alzheimer′s disease. Mutations of the APP gene lead to the early onset of Alzheimer′s disease and hereditary cerebral hemorrhage with amyloidosis.

Physical form

Format: Purified
Protein A Purified mouse immunoglobulin in 20 mM sodium phosphate, 250 mM NaCl, pH. 7.6, with 0.1% sodium azide as a preservative.
Protein A purified

Preparation Note

Maintain for 1 year at 2–8°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
Brain tissue, brain cell lysates

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.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 2

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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Deletion of Mint proteins decreases amyloid production in transgenic mouse models of Alzheimer's disease.
Ho, A; Liu, X; Sudhof, TC
The Journal of Neuroscience null
Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.
Atamna, H; Killilea, DW; Killilea, AN; Ames, BN
Proceedings of the National Academy of Sciences of the USA null
Gene expression profiles of APP and BACE1 in Tg SOD1G93A cortical cells.
O Spadoni, A Crestini, P Piscopo, L Malvezzi-Campeggi, I Carunchio, M Pieri, C Zona, A Confaloni
Cellular and Molecular Neurobiology null
Generation and initial characterization of FDD knock in mice.
Giliberto, L; Matsuda, S; Vidal, R; D'Adamio, L
Testing null
GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.
Li, Yazhou, et al.
Journal of Alzheimer'S Disease, 19, 1205-1219 (2010)
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