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S4316

Sigma-Aldrich

Amyloid Precursor Protein β, Secreted human

recombinant, expressed in E. coli (N-terminal histidine tagged), solution

Sinónimos:

Amyloid Precursor Protein β, Secreted, sAPPβ

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About This Item

MDL number:
UNSPSC Code:
12352202
NACRES:
NA.32

recombinant

expressed in E. coli (N-terminal histidine tagged)

Quality Level

form

solution

mol wt

~100 kDa by SDS-PAGE

UniProt accession no.

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... APP(351)

General description

Amyloid-β (Aβ) peptides are a major component of the senile plaques characteristic of the Alzheimer brain. It is a type- I transmembrane protein. The gene encoding amyloid-β is localized on human chromosome 21.

Application

Human amyloid precursor protein β has been used as peptide standard.

Biochem/physiol Actions

The secreted amyloid precursor β (sAPPβ) is a proteolytic cleavage product of β amyloid precursor protein (APP). APP is cleaved by β-secretase into two fragments, sAPPβ and β-amyloid peptide (Aβ). The Aβ is a component of amyloid plaques, one of the major hallmarks of Alzheimer`s disease (AD), while the sAPPβ is thought to modulate neuronal function and cell survival. Mutation in APP found in Swedish familial AD pedigree increases the susceptibility of APP to β-secretase cleavage and the formation of Aβ and sAPPβ. In contrast, activation of protein kinase C (PKC) decreases the levels of sAPPβ. The trans-Golgi network (TGN) is the major site for β-secretase activity.

Physical form

0.2 μm filtered solution in 20 mM Tris (pH 7.4), 0.5 M NaCl, 1 mM EDTA, 5 mM βME, 2 μg/ml aprotinin

Preparation Note

sAPPβ was expressed in E. coli as a soluble protein and purified under non-denaturing conditions

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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D J Selkoe
Nature, 399(6738 Suppl), A23-A31 (1999-07-07)
Studies of the molecular basis of Alzheimer's disease exemplify the increasingly blurred distinction between basic and applied biomedical research. The four genes so far implicated in familial Alzheimer's disease have each been shown to elevate brain levels of the self-aggregating
Conformational Dynamics of Specific A? Oligomers Govern Their Ability To Replicate and Induce Neuronal Apoptosis.
Dean DN
Biochemistry (2016)
Regulation of global gene expression and cell proliferation by APP.
Wu Y
Scientific Reports (2016)
In vivo BACE1 inhibition leads to brain A? lowering and increased a-secretase processing of APP without effect on Neuregulin-1
Sethu Sankaranarayanan
Journal of Pharmacology and Experimental Therapeutics (2018)
C Haass et al.
Nature, 357(6378), 500-503 (1992-06-11)
Progressive cerebral deposition of the amyloid beta-peptide is an early and invariant feature of Alzheimer's disease. The beta-peptide is released by proteolytic cleavages from the beta-amyloid precursor protein (beta APP), a membrane-spanning glycoprotein expressed in most mammalian cells. Normal secretion

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