SCP0048
Amyloid β 42-1 reverse human
≥95% (HPLC)
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About This Item
Fórmula empírica (notación de Hill):
C203H311N55O60S1
Peso molecular:
4514.04
UNSPSC Code:
12352200
NACRES:
NA.32
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assay
≥95% (HPLC)
form
lyophilized
composition
Peptide Content, ≥75%
storage condition
protect from light
storage temp.
−20°C
Amino Acid Sequence
Ala-Ile-Val-Val-Gly-Gly-Val-Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly-Val-Asp-Glu-Ala-Phe-Phe-Val-Leu-Lys-Gln-His-His-Val-Glu-Tyr-Gly-Ser-Asp-His-Arg-Phe-Glu-Ala-Asp
Application
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.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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S M Yatin et al.
Neurobiology of aging, 20(3), 325-330 (1999-12-10)
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Journal of Alzheimer's disease : JAD, 64(3), 957-971 (2018-07-12)
Alzheimer's disease (AD) is characterized by neuritic plaques and neurofibrillary tangles. It is reported that enzymatic degradation of amyloid-β (Aβ) plays a pivotal role in Aβ accumulation and type-2 cannabinoid receptor (CB2R) participates in Aβ processing in the brain; however
U Igbavboa et al.
Neuroscience, 142(3), 655-660 (2006-08-15)
Amyloid beta-protein (Abeta) increases apolipoprotein E (apoE) levels in astrocytes which could alter lipid trafficking. The mechanism for the Abeta-induced increase in apoE levels is not well understood. It is well established that stimulation of beta-adrenergic receptors (betaARs) increases cAMP
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