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Merck
CN
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文件

14-536

Sigma-Aldrich

MAP Kinase 2/Erk2 Protein, inactive, Human, 50 g

Unactive, N-terminal GST-tagged, recombinant human full length MAP Kinase 2, for use in Kinase Assays.

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UNSPSC代码:
12352200
eCl@ss:
32160405
NACRES:
NA.41

生物来源

human

质量水平

100

重组

expressed in E. coli

分子量

Mw 67.8 kDa

制造商/商品名称

Upstate®

技术

activity assay: suitable (kinase)

NCBI登记号

NM_002745.4
NM_138957.2

UniProt登记号

P28482

运输

dry ice

一般描述

N-terminal GST-tagged, recombinant human full length MAP Kinase 2
Product Source: Expressed in E. coli

应用

Research Category
Metabolism

Inflammation & Immunology
Research Sub Category
Obesity

Metabolic Disorders

Osteoporosis

Arthritis

生化/生理作用

Protein Target: MAPK2
Target Sub-Family: CMGC

质量

routinely evaluated by phosphorylation of MBP substrate

外形

Glutathione agarose affinity chromatography

储存及稳定性

6 months at -20°C

其他说明

For Specific Activity data, refer to the Certificate of Analysis for individual lots of this enzyme.

法律信息

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

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.

象形图

Exclamation mark
GHS07

警示用语：

Warning

危险声明

H317

危险分类

Skin Sens. 1

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable

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Xiaoyun Wang et al.
Scientific reports, 6, 28260-28260 (2016-06-16)
Although the translational function of tRNA has long been established, extra translational functions of tRNA are still being discovered. We previously developed a computational method to systematically predict new tRNA-protein complexes and experimentally validated six candidate proteins, including the mitogen-activated
Ivana Yen et al.
Cancer cell, 34(4), 611-625 (2018-10-10)
Targeting KRAS mutant tumors through inhibition of individual downstream pathways has had limited clinical success. Here we report that RAF inhibitors exhibit little efficacy in KRAS mutant tumors. In combination drug screens, MEK and PI3K inhibitors synergized with pan-RAF inhibitors

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