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Merck
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Key Documents

12-555

Sigma-Aldrich

Crosstide KK

Crosstide KK primarily used in Kinase Assays.

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About This Item

UNSPSC Code:
12352202
eCl@ss:
32160405
NACRES:
NA.42

Quality Level

manufacturer/tradename

Upstate®

technique(s)

activity assay: suitable (kinase)

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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D Konrad et al.
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.
D R Alessi et al.
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
R Somwar et al.
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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