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Key Documents

B0806

Sigma-Aldrich

Anti-BACE 1, C-Terminus (485-501) antibody produced in rabbit

enhanced validation

affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-β-Site APP Cleaving Enzyme

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.43

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 70 kDa

Espèces réactives

human

Validation améliorée

recombinant expression
Learn more about Antibody Enhanced Validation

Technique(s)

microarray: suitable
western blot: 1:1,000 using a whole cell extract from the human kidney HEK293 cell line stably transfected with human BACE-1

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... BACE1(23621)

Description générale

BACE-1 (β-site APP cleaving enzyme, Asp2 or memapsin 2) is known as β-secretase. BACE-1 is highly expressed in neurons, the major site of Aβ generation. BACE-1 is localized within the Golgi and endosomal compartments, among the several intracellular sites where Aβ is thought to be produced. It constitutes the predominant β-secretase activity in human brain tissue.

Immunogène

synthetic peptide corresponding to the C-terminus of human BACE-1 (amino acids 485-501).

Application

Anti-BACE 1, C-Terminus (485-501) antibody produced in rabbit has been used in western blotting.

Actions biochimiques/physiologiques

Overexpression of β-site APP cleaving enzyme (BACE-1) leads to increased β-secretase activity while displaying appropriate cleavage site specificity for amyloid precursor protein (APP).

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 15 mM sodium azide.

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Marcus O W Grimm et al.
International journal of molecular sciences, 17(11) (2016-11-02)
One of the characteristics of Alzheimer´s disease (AD) is an increased amyloid load and an enhanced level of reactive oxidative species (ROS). Vitamin E has known beneficial neuroprotective effects, and previously, some studies suggested that vitamin E is associated with
Docosahexaenoic acid reduces amyloid beta production via multiple pleiotropic mechanisms
Grimm MOW, et al.
Test, 286(16), 14028-14039 (2011)
S Prasad Gabbita et al.
PloS one, 10(10), e0137305-e0137305 (2015-10-06)
Cytokines such as TNFα can polarize microglia/macrophages into different neuroinflammatory types. Skewing of the phenotype towards a cytotoxic state is thought to impair phagocytosis and has been described in Alzheimer's Disease (AD). Neuroinflammation can be perpetuated by a cycle of
Marcus O W Grimm et al.
The Journal of biological chemistry, 283(17), 11302-11311 (2008-03-01)
The major molecular risk factor for Alzheimer disease so far identified is the amyloidogenic peptide Abeta(42). In addition, growing evidence suggests a role of cholesterol in Alzheimer disease pathology and Abeta generation. However, the cellular mechanism of lipid-dependent Abeta production
Tatjana L Rothhaar et al.
TheScientificWorldJournal, 2012, 141240-141240 (2012-05-02)
Lipids play an important role as risk or protective factors in Alzheimer's disease (AD). Previously it has been shown that plasmalogens, the major brain phospholipids, are altered in AD. However, it remained unclear whether plasmalogens themselves are able to modulate

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