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Merck
CN

MABN10

Anti-Beta (β)-Amyloid antibody

mouse monoclonal, WO2

别名:

Alzheimer disease, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, Protease nexin-II, amyloid beta (A4) precursor protein, amyloid beta A4 protein, amyloid beta precursor protein, beta-amyloid peptide, human mRNA for amyloid A4 prec

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关于此项目

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Clone:
WO2, monoclonal
Species reactivity:
mouse, human
Application:
ELISA, IHC, WB
Citations:
47
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产品名称

抗-淀粉样蛋白β抗体,克隆W0-2, clone WO2, from mouse

biological source

mouse

antibody form

purified immunoglobulin

clone

WO2, monoclonal

species reactivity

mouse, human

technique(s)

ELISA: suitable, immunohistochemistry: suitable (paraffin), western blot: suitable

isotype

IgG2aκ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... APP(351)

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General description

与阿尔茨′海默病(AD)相关的脑和血管斑块主要由淀粉样蛋白β肽(Aβ)组成。Aβ衍生自淀粉样蛋白前体蛋白(APP)的切割,长度在39至43个氨基酸之间变化。Aβ [1-40]、Aβ [1-42]和Aβ [1-43]肽分别来自残基40、42和43后APP的裂解。切割是在最后一个APP处理步骤中通过γ-分泌酶进行的。Aβ[1-40]、[1-42]和[1-43]肽是AD中发生的斑块和缠结的主要成分。这些淀粉样蛋白β抗体和肽已被开发为阐明AD生物学的工具。
该抗体还能在人类阿尔茨海默病脑裂解液的蛋白质印迹上显示120和105 kDa的APP蛋白和~45 kDa的淀粉样蛋白低聚物。

Immunogen

人淀粉样β肽
表位:氨基酸残基4-10

Application

研究类别
神经科学
使用经验证可用于WB、IH、ELISA的该抗淀粉样蛋白β抗体(克隆G2-2)检测淀粉样蛋白β。
免疫组化分析: 一个先前批次以1:500稀释度在阿尔茨海默病的海马组织中检测到淀粉样蛋白β。
研究子类别
神经退行性疾病

Biochem/physiol Actions

该抗体可识别人淀粉样蛋白β的氨基酸残基4-10。

Physical form

形式:纯化
纯化的小鼠单克隆IgG2aκ,溶于含有0.1 M Tris-甘氨酸(pH 7.4,150 mM NaCl)和0.05%叠氮化钠的缓冲液中。
蛋白G纯化

Preparation Note

自收到之日起,在2-8°C条件下可稳定保存1年。

Analysis Note

对照
人类阿尔茨海默病脑组织裂解物
通过蛋白质印迹法对人阿尔茨海默病脑组织裂解物进行评估。

蛋白质印迹分析:0.5 µg/ml的该抗体在10 µg人阿尔茨海默病脑组织裂解物中检测到淀粉样蛋白β。

Other Notes

替代:MAB1561
浓度:请参考批次特异性浓缩物的检验报告。

Disclaimer

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Luisa Diomede et al.
Neurobiology of disease, 62, 521-532 (2013-11-05)
Although Alzheimer's disease (AD) is usually sporadic, in a small proportion of cases it is familial and can be linked to mutations in β-amyloid precursor protein (APP). Unlike the other genetic defects, the mutation [alanine-673→valine-673] (A673V) causes the disease only
Yuhai Zhao et al.
Frontiers in aging neuroscience, 8, 140-140 (2016-07-06)
One prominent and distinguishing feature of progressive, age-related neurological diseases such as Alzheimer's disease (AD) and prion disease (PrD) is the gradual accumulation of amyloids into dense, insoluble end-stage protein aggregates. These polymorphic proteolipid lesions are known to contribute to
Deficits in the miRNA-34a-regulated endogenous TREM2 phagocytosis sensor-receptor in Alzheimer's disease (AD); an update.
Bhattacharjee, S; Zhao, Y; Lukiw, WJ
Frontiers in Aging Neuroscience null
Eitan Wong et al.
Proceedings of the National Academy of Sciences of the United States of America, 116(13), 6385-6390 (2019-03-10)
The mechanism by which γ-secretase activating protein (GSAP) regulates γ-secretase activity has not yet been elucidated. Here, we show that knockout of GSAP in cultured cells directly reduces γ-secretase activity for Aβ production, but not for Notch1 cleavage, suggesting that
Lina M Vargas et al.
PloS one, 9(3), e92309-e92309 (2014-03-25)
The early stages of Alzheimer's disease are characterised by impaired synaptic plasticity and synapse loss. Here, we show that amyloid-β oligomers (AβOs) activate the c-Abl kinase in dendritic spines of cultured hippocampal neurons and that c-Abl kinase activity is required

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