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AB5076

Sigma-Aldrich

Anti-Amyloid Antibody, β 1-40/42

serum, Chemicon®

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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

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human, mouse

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... APP(351)

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This Item
AB1510MAB5206MAB5208
Sigma-Aldrich

AB5076

Anti-Amyloid Antibody, β 1-40/42

Quality Level

100

Quality Level

100

Quality Level

300

Quality Level

100

antibody form

serum

antibody form

serum

antibody form

culture supernatant

antibody form

purified immunoglobulin

clone

polyclonal

clone

polyclonal

clone

DE2, monoclonal

clone

AB10, monoclonal

UniProt accession no.

P05067

UniProt accession no.

P05067

UniProt accession no.

P05067

UniProt accession no.

P05067

species reactivity

human, mouse

species reactivity

human

species reactivity

monkey, bovine, human

species reactivity

human, monkey, bovine

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Specificity

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.

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
Research Sub Category
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.

Linkage

Replaces: AB5408

Physical form

Rabbit Serum. Liquid and 0.1% sodium azide.
Unpurified

Storage and Stability

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

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 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Roberto Piacentini et al.
Scientific reports, 5, 15444-15444 (2015-10-22)
Increasing evidence suggests that recurrent Herpes Simplex Virus type 1 (HSV-1) infection spreading to the CNS is a risk factor for Alzheimer's Disease (AD) but the underlying mechanisms have not been fully elucidated yet. Here we demonstrate that in cultured
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
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
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
Xinhua Zhan et al.
Journal of Alzheimer's disease : JAD, 46(2), 507-523 (2015-03-21)
Ischemia, white matter injury, and Alzheimer's disease (AD) pathologies often co-exist in aging brain. How one condition predisposes to, interacts with, or perhaps causes the others remains unclear. To better understand the link between ischemia, white matter injury, and AD

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