SKL2001

SKL2001通过增加细胞内β-catenin蛋白水平，上调β-catenin反应性转录，同时抑制了β-catenin在Ser33/37/Thr41和Ser45位点的磷酸化，阻止了其被标记为蛋白酶体降解，而不影响CK1和GSK-3β酶活性。SKL2001破坏了Axin/β-catenin之间的相互作用，这一步骤对于CK1和GSK-3β介导的β-catenin在Ser33/37/Thr41和Ser45的磷酸化至关重要。SKL2001对间充质干细胞的处理促进了成骨细胞的形成并抑制了脂肪细胞的分化，这两个过程都伴随着Wnt/β-catenin途径的激活。SKL2001既不影响NF-κB或p53报告活性，也不影响GSK-3β活性，但抑制β-catenin的磷酸化[1]。

DMSO:50 mg/mL (174.65 mM);Ethanol:53 mg/mL (185.13 mM);H2O:< 1 mg/mL (insoluble or slightly soluble)

The HEK293 reporter and control cell lines were established. The HEK293 reporter cells were inoculated into 384-well plates at 10 000 cells per well and grown for 24 h. Next, each compound in the chemical library (～270 000) was added to at a final concentration of 20 μM. After 15 h, the plates were assayed for firefly luciferase activity.(Only for Reference)