14-515
MAP Kinase 1/Erk1 Protein, inactive, 50 g
Unactive, N-terminal GST-tagged, recombinant, full-length, human MAP Kinase 1/Erk1, for use in Kinase Assays.
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About This Item
UNSPSC Code:
12352202
eCl@ss:
32160405
NACRES:
NA.32
Pricing and availability is not currently available.
Recommended Products
biological source
human
Quality Level
recombinant
expressed in E. coli
mol wt
Mw 70 kDa
manufacturer/tradename
Upstate®
technique(s)
activity assay: suitable (kinase)
NCBI accession no.
UniProt accession no.
shipped in
dry ice
General description
N-terminal GST-tagged, recombinant, full-length, human MAP Kinase 1/Erk1
Product Source: expressed in E. coli
Application
Research Category
Metabolism
Metabolism
Research Sub Category
Obesity
Metabolic Disorders
Obesity
Metabolic Disorders
Biochem/physiol Actions
Protein Target: MAPK1
Target Sub-Family: CMGC
Quality
routinely evaluated by phosphorylation of MBP substrate in vitro
Physical form
Glutathione-agarose
Storage and Stability
6 months at -20°C
Other Notes
For Specific Activity data, refer to the Certificate of Analysis for individual lots of this enzyme.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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.
Signal Word
Warning
Hazard Statements
Precautionary Statements
Hazard Classifications
Skin Sens. 1
Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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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