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生物来源
mouse
质量水平
偶联物
unconjugated
抗体形式
purified immunoglobulin
抗体产品类型
primary antibodies
克隆
mN1A, monoclonal
形式
buffered aqueous solution
种属反应性
human, mouse
浓度
1 mg/mL
技术
flow cytometry: suitable
immunoblotting: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
immunoprecipitation (IP): suitable
同位素/亚型
IgG1
NCBI登记号
UniProt登记号
应用
research pathology
research pathology
运输
wet ice
储存温度
2-8°C
靶向翻译后修饰
unmodified
基因信息
human ... NOTCH1(4851)
相关类别
一般描述
The mouse monoclonal antibody mN1A recognizes intracellular domain of Notch 1 protein, mainly its activated form. The unprocessed Notch 1 protein is recognized with lower affinity.
免疫原
GST fusion protein containing cdc10-NCR region of mouse Notch1
特点和优势
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
外形
Solution in phosphate buffered saline, pH 7.4, with 15 mM sodium azide.
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
Frontiers in cellular neuroscience, 9, 447-447 (2015-12-05)
Notch signaling plays a crucial role in adult brain function such as synaptic plasticity, memory and olfaction. Several reports suggest an involvement of this pathway in neurodegenerative dementia. Yet, to date, the mechanism underlying Notch activity in mature neurons remains
Cell death and differentiation, 22(11), 1775-1784 (2015-03-31)
Neurological disorders such as Alzheimer's disease, stroke and epilepsy are currently marred by the lack of effective treatments to prevent neuronal death. Erroneous cell cycle reentry (CCR) is hypothesized to have a causative role in neurodegeneration. We show that forcing
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