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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

Synonym(s):

Anti-β-Site APP Cleaving Enzyme

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About This Item

MDL number:
MFCD03454775
UNSPSC Code:
12352203
NACRES:
NA.43

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 70 kDa

species reactivity

human

enhanced validation

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

UniProt accession no.

P56817

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... BACE1(23621)

Related Categories

General description

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.

Immunogen

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.

Biochem/physiol Actions

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).

Physical form

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

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

nwg

flash_point_f

Not applicable

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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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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