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Merck
CN

MAB5206

Anti-Beta (β)-Amyloid antibody

CHEMICON®, mouse monoclonal, DE2

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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-Amyloid Antibody, β 1-16, clone DE2, culture supernatant, clone DE2, Chemicon®

biological source

mouse

antibody form

culture supernatant

antibody product type

primary antibodies

clone

DE2, monoclonal

species reactivity

monkey, bovine, human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable

isotype

IgG

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

Quality Level

300

Gene Information

human ... APP(351)

Application

Anti-Amyloid Antibody, β 1-16, clone DE2 is an antibody against Amyloid for use in ELISA, WB, IH(P).
Western blot: 1:10-1:300 Immunohistochemistry: 1:10-1:200 on formaldehyde fixed, paraffin embedded tissue, requires formic acid or microwave pretreatment to stain Alzheimer′s brain senile plaques. ELISA Immunoprecipitation

Optimal working dilutions must be determined by end user.

Physical form

Culture supernatant. Liquid containing 0.02% sodium azide.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk

WGK 1

Certificates of Analysis (COA)

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Mélanie Sipion et al.
Scientific reports, 13(1), 19828-19828 (2023-11-15)
Photobiomodulation (PBM), the process of exposing tissue to red or near-infrared light, has become a topic of great interest as a therapy for diverse pathologies, including neurodegenerative disorders. Here, we aimed to evaluate the potential beneficial effect of PBM on
S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.
Kim, HJ; Chang, KA; Ha, TY; Kim, J; Ha, S; Shin, KY; Moon, C; Nacken, W; Kim, HS; Suh, YH
Testing null
Avindra Nath et al.
Neuromolecular medicine, 3(1), 29-39 (2003-04-01)
Studies of amyloid precursor protein transgenic mice suggest that immune responses to amyloid beta peptide (Abeta) may be instrumental in the removal of plaques from the brain, but the initial clinical trial of an Abeta vaccine in patients with Alzheimer
Alexander J Ehrenberg et al.
Acta neuropathologica, 141(5), 651-666 (2021-03-08)
The farnesyltransferase inhibitor, Lonafarnib, reduces tau inclusions and associated atrophy in familial tauopathy models through activation of autophagy, mediated by the inhibition of farnesylation of the Ras GTPase, Rhes. While hinting at a role of Rhes in tau aggregation, it
Ji-Hye L Hwang et al.
Acta neuropathologica, 145(1), 1-12 (2022-12-06)
Tuberous sclerosis complex (TSC) is a neurogenetic disorder leading to epilepsy, developmental delay, and neurobehavioral dysfunction. The syndrome is caused by pathogenic variants in TSC1 (coding for hamartin) or TSC2 (coding for tuberin). Recently, we reported a progressive frontotemporal dementia-like
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