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Documentos Principais

AB5076

Sigma-Aldrich

Anti-Amyloid Antibody, β 1-40/42

serum, Chemicon®

Sinônimo(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

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About This Item

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

fonte biológica

rabbit

Nível de qualidade

forma do anticorpo

serum

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

reatividade de espécies

human, mouse

fabricante/nome comercial

Chemicon®

técnica(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

nº de adesão UniProt

Condições de expedição

dry ice

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... APP(351)

Especificidade

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.

Imunogênio

A synthetic beta-amyloid peptide 1-40 conjugated to BSA.

Aplicação

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.

Ligação

Replaces: AB5408

forma física

Rabbit Serum. Liquid and 0.1% sodium azide.
Unpurified

Armazenamento e estabilidade

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.

Nota de análise

Control
Alzheimer′s disease brain tissue, whole tissue extracts from mouse brain

Outras notas

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informações legais

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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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
The effect of exogenous cholesterol and lipid-modulating agents on enterocytic amyloid-beta abundance.
Pallebage-Gamarallage, MM; Galloway, S; Johnsen, R; Jian, L; Dhaliwal, S; Mamo, JC
The British Journal of Nutrition null
Probucol suppresses enterocytic accumulation of amyloid-I? induced by saturated fat and cholesterol feeding.
Menuka M Pallebage-Gamarallage,Susan Galloway,Ryusuke Takechi,Satvinder Dhaliwal,John C L Mamo
Lipids null
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
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

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