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Merck
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Key Documents

SCP0048

Sigma-Aldrich

淀粉样蛋白β 42-1逆转人类

≥95% (HPLC)

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About This Item

经验公式（希尔记法）:
C203H311N55O60S1
分子量:
4514.04
分類程式碼代碼:
12352200
NACRES:
NA.32

化驗

≥95% (HPLC)

形狀

lyophilized

成份

Peptide Content, ≥75%

儲存條件

protect from light

儲存溫度

−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

應用

淀粉样β（Aβ）是指衍生自淀粉样蛋白前体蛋白的肽，其长度在36-43个氨基酸之间变化。 Aβ（s）肽，其肽片段和突变片段用于研究广泛的代谢和调节功能，包括激酶的激活、胆固醇转运的调节、作为转录因子的功能和炎症的调节因子。 Aβ（s）肽及其肽片段还用于研究氧化应激、金属结合和蛋白质交联机制，例如阿尔茨海默病和神经变性。

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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Kodeeswaran Parameshwaran et al.
Synapse (New York, N.Y.), 61(6), 367-374 (2007-03-21)
The brains of Alzheimer's disease (AD) patients have large numbers of plaques that contain amyloid beta (Abeta) peptides which are believed to play a pivotal role in AD pathology. Several lines of evidence have established the inhibitory role of Abeta
S M Yatin et al.
Neurobiology of aging, 20(3), 325-330 (1999-12-10)
The amyloid beta-peptide (A beta)-associated free radical oxidative stress model for neuronal death in Alzheimer's disease (AD) brain predicts that neuronal protein oxidation is a consequence of A beta-associated free radicals [8]. In this study we have used both in
Lin Wang et al.
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
Hong Lian et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 36(2), 577-589 (2016-01-14)
Increasing evidence supports a role of neuroinflammation in the pathogenesis of Alzheimer's disease (AD). Previously, we identified a neuron-glia signaling pathway whereby Aβ acts as an upstream activator of astroglial nuclear factor kappa B (NF-κB), leading to the release of

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