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Merck
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Documenti fondamentali

SCP0049

Sigma-Aldrich

[Gln22]-Amyloid β 1-40 human

≥95% (HPLC)

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About This Item

Formula empirica (notazione di Hill):
C194H296N54O57S1
Peso molecolare:
4328.82
Codice UNSPSC:
12352209
NACRES:
NA.77

Saggio

≥95% (HPLC)

Stato

lyophilized

Composizione

Peptide Content, ≥70%

Condizioni di stoccaggio

protect from light

Temperatura di conservazione

−20°C

Categorie correlate

Amino Acid Sequence

Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Gln-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val

Applicazioni

Amyloid β (Aβ) refers to peptides derived from Amyloid precursor protein that vary in length from 36-43 amino acids. Aβ(s) peptides, their peptide fragments and mutated fragments are used to study a wide range of metabolic and regulatory functions including activation of kinases, regulation of cholesterol transport, function as a transcription factor, and regulators of inflammation. Aβ(s) peptides and their peptide fragments are also used to study oxidative stress, metal binding and mechanisms of protein cross-linking in the context of diseases such as Alzheimer′s disease and neurodegeneration.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

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Certificati d'analisi (COA)

Lot/Batch Number
BB0626

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Régis Blaise et al.
Aging cell, 11(3), 384-393 (2012-01-21)
Cerebral amyloid angiopathy (CAA) is an important cause of intracerebral hemorrhages in the elderly, characterized by amyloid-β (Aβ) peptide accumulating in central nervous system blood vessels. Within the vessel walls, Aβ-peptide deposits [composed mainly of wild-type (WT) Aβ(1-40) peptide in
Masakazu Hashimoto et al.
Journal of neuroscience methods, 205(2), 364-367 (2012-02-14)
Several lines of evidence suggest that aggregation of the amyloid β-peptide (Aβ) in the brain is a trigger of Alzheimer's disease (AD). Thus, quantification of Aβ in several different types of samples from brain is fundamental for understanding AD pathogenesis.
Hye Jung Kim et al.
Journal of neurochemistry, 121(2), 228-238 (2012-02-23)
Amyloid β-protein (Aβ) deposits in brains of Alzheimer's disease patients generate proinflammatory cytokines and chemokines that recruit microglial cells to phagocytose Aβ. Nucleotides released from apoptotic cells activate P2Y(2) receptors (P2Y(2) Rs) in macrophages to promote clearance of dead cells.
Olujide O Olubiyi et al.
The journal of physical chemistry. B, 116(10), 3280-3291 (2012-02-04)
In this simulation study, we present a comparison of the secondary structure of the two major alloforms of the Alzheimer's peptide (Aβ(1-40) and Aβ(1-42)) on the basis of molecular dynamics (MD) simulations on thea microsecond time scale using the two

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