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SCP0038

Sigma-Aldrich

Amyloid β 1-42 rat

≥90% (HPLC)

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About This Item

Empirical Formula (Hill Notation):
C199H307N53O59S1
Molecular Weight:
4417.95
UNSPSC Code:
12352200
NACRES:
NA.32

assay

≥90% (HPLC)

form

lyophilized

composition

Peptide Content, ≥75%

storage condition

protect from light

storage temp.

−20°C

Amino Acid Sequence

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

General description

Amyloid β (Aβ) 1-42 is the major Aβ species in the amyloid plaques that develop in the case of Alzheimer′s disease (AD). It has a cross-β structure with parallel, in-register β-sheets.

Application

Amyloid β 1-42 rat has been used as an amyloid β (Aβ) oligomer in intracerebroventricular (ICV) injection/intra-hippocampal infusion to establish the Alzheimer′s disease (AD) model in rat.

Biochem/physiol Actions

Amyloid β 1-42 forms amyloid fibrils more readily compared to Aβ(1–40), in vitro. Aβ1-42 injections are known to cause brain dysfunction indicating learning and memory deficits. Amyloid β (Aβ) refers to peptides derived from amyloid precursor protein that vary in length from 37–43 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.

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Jing Wang et al.
Molecular medicine reports, 23(6) (2021-04-22)
Ginkgolide B (GB), the diterpenoid lactone compound isolated from the extracts of Ginkgo biloba leaves, significantly improves cognitive impairment, but its potential pharmacological effect on astrocytes induced by β‑amyloid (Aβ)1‑42 remains to be elucidated. The present study aimed to investigate the
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