12-555
Crosstide KK
Crosstide KK primarily used in Kinase Assays.
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About This Item
Quality Level
manufacturer/tradename
Upstate®
technique(s)
activity assay: suitable (kinase)
NCBI accession no.
UniProt accession no.
shipped in
wet ice
Gene Information
human ... SGK3(23678)
Biochem/physiol Actions
Protein Target: SGK3
Target Sub-Family: AGC
Quality
Routinely evaluated by phosphorylation using SGK3, active (Catalog # 14-647).
Storage and Stability
2 years at 4°C
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.
Storage Class Code
11 - Combustible Solids
WGK
WGK 1
Certificates of Analysis (COA)
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Find documentation for the products that you have recently purchased in the Document Library.
Diabetes, 50(6), 1464-1471 (2001-05-26)
The cofactor of mitochondrial dehydrogenase complexes and potent antioxidant alpha-lipoic acid has been shown to lower blood glucose in diabetic animals. alpha-Lipoic acid enhances glucose uptake and GLUT1 and GLUT4 translocation in 3T3-L1 adipocytes and L6 myotubes, mimicking insulin action.
The EMBO journal, 15(23), 6541-6551 (1996-12-02)
Insulin activated endogenous protein kinase B alpha (also known as RAC/Akt kinase) activity 12-fold in L6 myotubes, while after transfection into 293 cells PKBalpha was activated 20- and 50-fold in response to insulin and IGF-1 respectively. In both cells, the
The Biochemical journal, 359(Pt 3), 639-649 (2001-10-24)
We previously reported that SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), attenuates insulin-stimulated glucose uptake without altering GLUT4 translocation. These results suggested that insulin might activate GLUT4 via a p38 MAPK-dependent pathway. Here we explore this hypothesis
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