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
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)
相关类别
Application
研究类别
神经科学
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
神经退行性疾病
Analysis Note
对照
人类阿尔茨海默病脑组织裂解物
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。
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。
Biochem/physiol Actions
该抗体可识别人淀粉样蛋白β的氨基酸残基4-10。
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。
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
Other Notes
替代：MAB1561
浓度：请参考批次特异性浓缩物的检验报告。
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。
存储类别
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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
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
Mahfuz B Khan et al.
Journal of neurovirology, 22(2), 179-190 (2015-09-27)
In the era of combined antiretroviral therapy (CART), many of the complications due to HIV-1 infection have diminished. One exception is HIV-associated neurocognitive disorder (HAND). HAND is a spectrum of disorders in cognitive function that ranges from asymptomatic disease to
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
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