重组人CREG1/CREG蛋白(ab131699)
Key features and details
- Expression system: Escherichia coli
- Purity: > 95% SDS-PAGE
- Tags: His tag N-Terminus
- Suitable for: SDS-PAGE, MS
描述
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产品名称
重组人CREG1/CREG蛋白
参阅全部 CREG1/CREG 蛋白酶 -
纯度
> 95 % SDS-PAGE.
ab131699 was purified using conventional chromatography techniques. -
表达系统
Escherichia coli -
Accession
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蛋白长度
Full length protein -
无动物成分
No -
性质
Recombinant -
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种属
Human -
序列
MGSSHHHHHH SSGLVPRGSH MGSMRGGRDH GDWDEASRLP PLPPREDAAR VARFVTHVSD WGALATISTL EAVRGRPFAD VLSLSDGPPG AGSGVPYFYL SPLQLSVSNL QENPYATLTM TLAQTNFCKK HGFDPQSPLC VHIMLSGTVT KVNETEMDIA KHSLFIRHPE MKTWPSSHNW FFAKLNITNI WVLDYFGGPK IVTPEEYYNV TVQ -
预测分子量
24 kDa including tags -
氨基酸
32 to 220 -
标签
His tag N-Terminus
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相关产品
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Related Products
技术指标
Our Abpromise guarantee covers the use of ab131699 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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应用
SDS-PAGE
Mass Spectrometry
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质谱法
MALDI-TOF -
形式
Liquid -
补充说明
This product was previously labelled as CREG1
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Concentration information loading...
制备和贮存
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稳定性和存储
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
pH: 8.00
Constituents: 0.32% Tris HCl, 10% Glycerol (glycerin, glycerine), 0.88% Sodium chloride
常规信息
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别名
- Cellular repressor of E1A stimulated genes 1
- Cellular repressor of E1A-stimulated genes 1
- CREG
see all -
功能
May contribute to the transcriptional control of cell growth and differentiation. Antagonizes transcriptional activation and cellular transformation by the adenovirus E1A protein. The transcriptional control activity of cell growth requires interaction with IGF2R. -
序列相似性
Belongs to the CREG family. -
翻译后修饰
N-glycosylated. -
细胞定位
Secreted. - Information by UniProt
图片
实验方案
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
数据表及文件
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SDS download
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Datasheet download
文献 (0)
ab131699 尚未被引用在任何文献中。