MABN11
Anti-Beta (β)-Amyloid antibody
mouse monoclonal, G2-10
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β40抗体，克隆G2-10, clone G2-10, from mouse
biological source
mouse
antibody form
purified antibody
clone
G2-10, monoclonal
species reactivity
human, mouse
technique(s)
ELISA: suitable
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2bκ
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
Analysis Note
对照
APP转基因CRND8小鼠脑裂解物
APP转基因CRND8小鼠脑裂解物
通过蛋白质印迹法在APP转基因CRND8小鼠脑裂解物中进行评估。
蛋白质印迹分析：1 µg/ml的该抗体在10 µg APP转基因CRND8小鼠脑裂解物上检测到淀粉样蛋白β40。
蛋白质印迹分析：1 µg/ml的该抗体在10 µg APP转基因CRND8小鼠脑裂解物上检测到淀粉样蛋白β40。
Application
使用经验证可用于WB、IH、ELISA的抗淀粉样蛋白β40抗体（克隆G2-10）检测淀粉样蛋白β40。
免疫组织化学分析： 一个先前批次以1:300稀释度在阿尔茨’海默病的海马组织中检测到淀粉样蛋白β40。
研究子类别
神经退行性疾病
神经退行性疾病
研究类别
神经科学
神经科学
Biochem/physiol Actions
该抗体可识别C末端的淀粉样蛋白β40。
Disclaimer
除非我们的目录或产品随附的其他公司文件中另有说明，否则我们的产品预期仅用于研究用途，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对人类或动物的任何类型的消费或应用。
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。Aβ抗体和肽已被开发为阐明AD生物学的工具。
约4 kDa
Immunogen
C末端的人淀粉样蛋白β40的线性肽。
表位：C末端
Other Notes
浓度：关于批次特定浓度请参见检验报告。
Physical form
形式：纯化
纯化的小鼠单克隆IgG2bκ，溶于含0.1 M Tris-甘氨酸（pH 7.4，150 mM NaCl）、0.05%叠氮化钠和1% BSA的缓冲液中。
纯化蛋白G
Preparation Note
自接收之日起，在2-8°C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
Ditte Z Christensen et al.
Frontiers in aging neuroscience, 6, 139-139 (2014-07-16)
Abnormalities and impairments in axonal transport are suggested to strongly contribute to the pathological alterations underlying AD. The exact mechanisms leading to axonopathy are currently unclear, but it was recently suggested that APP expression itself triggers axonal degeneration. We used
Ge Li et al.
International journal of molecular medicine, 42(4), 1935-1944 (2018-08-08)
Aging is associated with impairment of the paravascular pathway caused by the activation of astrocytes and depolarization of protein aquaporin‑4 (AQP4) water channels, resulting in the accumulation of protein waste, including amyloid β (Aβ), in the brain parenchyma. The secreted
Jin Cui et al.
Cell discovery, 1, 15021-15021 (2015-01-01)
Despite decades of intense global effort, no disease-modifying drugs for Alzheimer's disease have emerged. Molecules targeting catalytic activities of γ-secretase or β-site APP-cleaving enzyme 1 (BACE1) have been beset by undesired side effects. We hypothesized that blocking the interaction between
Kevin Kleffman et al.
Cancer discovery, 12(5), 1314-1335 (2022-03-10)
Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate
Vanessa Kurth et al.
The Journal of biological chemistry, 299(8), 104997-104997 (2023-07-03)
Presenilin-1 (PSEN1) is the catalytic subunit of the intramembrane protease γ-secretase and undergoes endoproteolysis during its maturation. Heterozygous mutations in the PSEN1 gene cause early-onset familial Alzheimer's disease (eFAD) and increase the proportion of longer aggregation-prone amyloid-β peptides (Aβ42 and/or
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