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Merck
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Key Documents

SCP0037

Sigma-Aldrich

淀粉样蛋白β1-40大鼠

≥95% (HPLC)

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About This Item

经验公式(希尔记法):
C190H291N51O57S1
分子量:
4233.72
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

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

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 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Xuehong Yu et al.
Neurobiology of learning and memory, 123, 168-178 (2015-06-14)
Single-session anodal transcranial direct current stimulation (tDCS) can improve the learning-memory function of patients with Alzheimer's disease (AD). After-effects of tDCS can be more significant if the stimulation is repeated regularly in a period. Here the behavioral and the histologic
Maryam Bagheri et al.
Neurobiology of learning and memory, 95(3), 270-276 (2010-12-15)
Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by increased β-amyloid (Aβ) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease
Aynun N Begum et al.
Journal of Alzheimer's disease : JAD, 15(4), 625-640 (2008-12-20)
The rat amyloid-beta (Abeta) intracerebroventricular infusion can model aspects of Alzheimer's disease (AD) and has predicted efficacy of therapies such as ibuprofen and curcumin in transgenic mouse models. High density lipoprotein (HDL), a normal plasma carrier of Abeta, is used
Lian Hong et al.
The journal of physical chemistry. B, 114(34), 11261-11271 (2010-08-10)
There is no consensus on the coordinating ligands for Cu(2+) by Abeta. However, the differences in peptide sequence between human and rat have been hypothesized to alter metal ion binding in a manner that alters Cu(2+)-induced aggregation of Abeta. Herein
Tania Araujo Viel et al.
Neurobiology of aging, 29(12), 1805-1814 (2007-06-16)
Although numerous inflammation pathways have been implicated in Alzheimer's disease, the involvement of the kallikrein-kinin system is still under investigation. We anatomically localized and quantified the density of kinin B(1) and B(2) receptors binding sites in the rat brain after

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