生物来源
mouse
质量水平
抗体形式
ascites fluid
抗体产品类型
primary antibodies
克隆
Syn211, monoclonal
种属反应性
human
包装
antibody small pack of 25 μL
制造商/商品名称
Upstate®
技术
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable
NCBI登记号
UniProt登记号
运输
ambient
靶向翻译后修饰
unmodified
基因信息
human ... SNCA(6622)
特异性
α-突触核蛋白
免疫原
全长重组人 α-突触核蛋白
应用
使用该抗 α-突触核蛋白抗体(克隆Syn211,经验证可用于 IP、WB、IH)检测 α-突触核蛋白。
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
质量
通过免疫印迹对阿尔茨海默氏病患病的人全脑裂解液进行了常规评估。
目标描述
~14.5kDa
联系
替代:04-1053
外形
腹水
储存及稳定性
在 -20°C 条件下可保存 2 年
法律信息
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
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。
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WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Molecular and cellular neurosciences, 120, 103729-103729 (2022-04-22)
Among the pathological events associated with the dopaminergic neurodegeneration characteristic of Parkinson's disease (PD) are the accumulation of toxic forms of α-synuclein and microglial activation associated with neuroinflammation. Although numerous other processes may participate in the pathogenesis of PD, the
Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 32(1), e13726-e13726 (2019-10-03)
A hallmark feature of Parkinson's disease (PD) is the build-up of α-synuclein protein aggregates throughout the brain; however α-synuclein is also expressed in enteric neurons. Gastrointestinal (GI) symptoms and pathology are frequently reported in PD, including constipation, increased intestinal permeability
Neuron-to-neuron ?-synuclein propagation in vivo is independent of neuronal injury.
Acta Neuropathologica Communications null
Characterization of cognitive deficits in rats overexpressing human alpha-synuclein in the ventral tegmental area and medial septum using recombinant adeno-associated viral vectors.
Testing null
Journal of neurochemistry, 137(5), 806-819 (2016-01-27)
In this study, we used proton-localized spectroscopy ((1) H-MRS) for the acquisition of the neurochemical profile longitudinally in a novel rat model of human wild-type alpha-synuclein (α-syn) over-expression. Our goal was to find out if the increased α-syn load in
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