产品名称
MEK1抗体, Upstate®, from rabbit
biological source
rabbit
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
species reactivity
mouse, rat, human
manufacturer/tradename
Upstate®
technique(s)
immunoprecipitation (IP): suitable, western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... MAP2K1(5604)
General description
45kDa
Immunogen
对应于人MEK1氨基酸2-18(PKKKPTPIQLNPAPDGS)的肽。
Application
研究子类别
MAP激酶
MAP激酶
研究类别
信号传导
信号传导
这种MEK1抗体经验证可用于IP、WB检测MEK1。
Biochem/physiol Actions
MEK1
根据序列同源性预测会与兔发生交叉反应。
Physical form
70%储存缓冲液(0.1M Tris-甘氨酸(pH 7.4)、0.15M NaCl、0.05%叠氮化钠)和30%甘油。
形式:纯化
纯化蛋白A
Preparation Note
在-20°C下可保存2年
Analysis Note
对照
阳性抗原对照:货号12-301,未刺激的A431细胞裂解液。 添加 2.5µL 2-巯基乙醇/100µL 裂解液,煮沸5分钟以还原制剂。在微凝胶每个泳道上样20µg经还原的裂解液 。
阳性抗原对照:货号12-301,未刺激的A431细胞裂解液。 添加 2.5µL 2-巯基乙醇/100µL 裂解液,煮沸5分钟以还原制剂。在微凝胶每个泳道上样20µg经还原的裂解液 。
通过免疫印迹法对A431和3T3/A31细胞的RIPA裂解液进行了常规评估。
Other Notes
替代:04-376
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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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存储类别
10 - Combustible liquids
wgk
WGK 1
Bacillus anthracis lethal toxin represses MMTV promoter activity through transcription factors.
Kang, Z; Webster Marketon, JI; Johnson, A; Sternberg, EM
Journal of Molecular Biology null
Shihui Liu et al.
The Journal of biological chemistry, 283(1), 529-540 (2007-11-03)
Anthrax lethal toxin (LT), a virulence factor secreted by Bacillus anthracis, is selectively toxic to human melanomas with the BRAF V600E activating mutation because of its proteolytic activities toward the mitogen-activated protein kinase kinases (MEKs). To develop LT variants with
Jason M Warfel et al.
Toxins, 3(10), 1278-1293 (2011-11-10)
Systemic anthrax disease is characterized by vascular leakage pathologies. We previously reported that anthrax lethal toxin (LT) induces human endothelial barrier dysfunction in a cell death-independent manner with actin stress fiber formation and disruption of adherens junctions (AJs). In the