Molecular Weight(MW): 286.29
SKL2001 is a novel agonist of the Wnt/β-catenin pathway. It disrupts the Axin/β-catenin interaction.
Cited by 13 Publications
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(D) Overexpression of CASC2 suppressed the protein expression of β-catenin, Cyclin-D1, and c-Myc in U251 cells and the effect could be reversed by SKL2001. (E) CASC2 overexpression restrained the proliferation, migration, and invasion capacity in U251 cells and SKL2001 could reverse the effect of CASC2.
Neuropsychiatr Dis Treat, 2017, 13:1805-1813. SKL2001 purchased from Selleck.
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|Description||SKL2001 is a novel agonist of the Wnt/β-catenin pathway. It disrupts the Axin/β-catenin interaction.|
SKL2001 upregulated β-catenin responsive transcription by increasing the intracellular β-catenin protein level and inhibited the phosphorylation of β-catenin at residues Ser33/37/Thr41 and Ser45, which would mark it for proteasomal degradation, without affecting CK1 and GSK-3β enzyme activities. SKL2001 disrupted the Axin/β-catenin interaction, which is a critical step for CK1- and GSK-3β-mediated phosphorylation of β-catenin at Ser33/37/Thr41 and Ser45. The treatment of mesenchymal stem cells with SKL2001 promoted osteoblastogenesis and suppressed adipocyte differentiation, both of which were accompanied by the activation of Wnt/β-catenin pathway. SKL2001 did not affect either NF-κB or p53 reporter activity and inhibits β-catenin phosphorylation without affecting GSK-3β activity.
|In vitro||DMSO||57 mg/mL (199.09 mM)|
|Ethanol||57 mg/mL (199.09 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+40% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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