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AB5580

Sigma-Aldrich

抗-SCN8A钠通道抗体

Chemicon®, from rabbit

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别名:
Sodium Channel Nav1.6, NaCh6, PN4, CerIII
UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物来源

rabbit

质量水平

抗体形式

affinity purified immunoglobulin

抗体产品类型

primary antibodies

克隆

polyclonal

纯化方式

affinity chromatography

种属反应性

rat, mouse

制造商/商品名称

Chemicon®

技术

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

NCBI登记号

UniProt登记号

运输

wet ice

靶向翻译后修饰

unmodified

基因信息

human ... SCN8A(6334)

一般描述

电压门控钠通道通过在轴突和树突中产生动作电位,在神经系统中对电信号传导起关键作用。至少有10个基因编码哺乳动物中的钠通道,但是区分这些亚型的特定生理作用尚不清楚。 Nav1.6高度集中在外周神经系统感觉轴突和运动轴突的Ranvier音符和中枢神经系统节点上。 由于其一致且受限的标记,抗-Nav1.6(AB5580)已被有效地用作Ranvier标记的节点。

特异性

识别Scn8a(Nav1.6)。该表位对应于Scn8a的II和III结构域之间的细胞内环。不与任何其他已知蛋白发生交叉反应。

物种反应性: 由于序列同源性,预期该抗体对小鼠(20/20)和人(19/20)也有效。其他物种尚未经过测试。

免疫原

对应于来自小鼠(登录号AAD20438)或大鼠(登录号AAC26014)Scn8a的氨基酸1042-1061的肽。

应用

使用经验证可用于IC、IH &WB的抗SCN8A钠通道抗体检测SCN8A钠通道。
蛋白质印迹:(1:200)在大鼠脑膜上使用ECL。

固定冷冻切片的免疫组化。

大鼠背根神经节原代培养的免疫细胞化学(1:100)

稀释液应使用载体蛋白(例如BSA(1-3%))制备

最佳工作稀释度必须由最终用户确定。

其他说明

浓度:请参考批次特异性浓缩物的分析证书。

法律信息

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

危险声明

预防措施声明

危险分类

Aquatic Chronic 3

WGK

WGK 3


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Jacy L Wagnon et al.
Neurology. Genetics, 3(4), e170-e170 (2017-07-14)
To determine the functional effect of SCN8A missense mutations in 2 children with intellectual disability and developmental delay but no seizures. Genomic DNA was analyzed by next-generation sequencing. SCN8A variants were introduced into the Nav1.6 complementary DNA by site-directed mutagenesis.
Ping Li et al.
eNeuro, 4(3) (2017-07-01)
The GABA-B receptor is densely expressed throughout the brain and has been implicated in many CNS functions and disorders, including addiction, epilepsy, spasticity, schizophrenia, anxiety, cognitive deficits, and depression, as well as various aspects of nervous system development. How one
Devid Damiani et al.
The Journal of comparative neurology, 520(7), 1406-1423 (2011-11-22)
Retinitis pigmentosa (RP) is a family of inherited diseases causing progressive photoreceptor death. Retinal ganglion cells (RGCs) form the biological substrate for various therapeutic approaches designed to restore vision in RP individuals. Assessment of survival and preservation of RGCs in
Yasmina Manso et al.
Glia, 66(1), 34-46 (2017-07-20)
Chronic cerebral hypoperfusion is a key mechanism associated with white matter disruption in cerebral vascular disease and dementia. In a mouse model relevant to studying cerebral vascular disease, we have previously shown that cerebral hypoperfusion disrupts axon-glial integrity and the
Christopher D Makinson et al.
Neuron, 93(5), 1165-1179 (2017-02-28)
Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of

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