SKL2001 is an agonist of the Wnt/β-catenin pathway. SKL2001 stabilizes intracellular β-catenin via disruption of the Axin/β-catenin interaction, and can be applied to regulate mesenchymal stem cell differentiation[1].
SKL2001 (5, 10, and 30μM; 3d) consistently induced the accumulation of intracellular β-catenin and inhibited the expression of C/EBPα and PPARγ. The exposure of 3T3-L1 and ST2 cells to SKL2001 resulted in a concentration-dependent decrease in lipid droplet accumulation in response to insulin[1]. SKL2001 (10, 30μM; 15h) 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[1].Treatment of ECs with SKL2001 at 30μM for 12h induced the expressions of MALAT1, ZO-1 and Occludin[2].
SKL2001 (6mg/kg; ip; 7d) treatment results in a decrease in the permeability of the aortic wall of the mice[2].In the doxorubicin mouse model, SKL2001 (4mg/kg; ip; 7d) stimulated rCFs to activate the Wnt/β-catenin pathway, inducing cardiac dysfunction and myocardial fibrosis in mice[3].
References:
[1]. Gwak J, Hwang S G, Park H S, et al. Small molecule-based disruption of the Axin/β-catenin protein complex regulates mesenchymal stem cell differentiation[J]. Cell research, 2012, 22(1): 237-247.
[2]. Yang F, Zhang Y, Zhu J, et al. Laminar flow protects vascular endothelial tight junctions and barrier function via maintaining the expression of long non-coding RNA MALAT1[J]. Frontiers in Bioengineering and Biotechnology, 2020, 8: 647.
[3]. Yuan M, Shi H, Wang B, et al. Targeting SOCS2 alleviates myocardial fibrosis by reducing nuclear translocation of β-catenin[J]. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 2024, 1871(7): 119804.
SKL2001是一种Wnt/β-catenin通路激动剂。SKL2001通过破坏Axin/β-catenin的相互作用稳定细胞内的β-catenin，可用于调控间充质干细胞分化[1]。
SKL2001（5、10、30μM；3d）能持续诱导细胞内β-catenin的积累，抑制C/EBPα和PPARγ的表达。将 3T3-L1 和 ST2 细胞暴露于SKL2001会导致对胰岛素反应的脂滴积聚的浓度依赖性减少[1]。SKL2001（10、30μM；15h）通过增加细胞内β-catenin蛋白水平上调β-catenin反应性转录，抑制β-catenin在Ser33/37/Thr41和Ser45残基的磷酸化[1]。用30μM的SKL2001处理EC细胞12h，可诱导MALAT1、ZO-1和Occludin的表达[2]。
SKL2001（6mg/kg；ip；7d）可降低小鼠主动脉壁的通透性[2]。在多柔比星小鼠模型中，SKL2001（4mg/kg；ip；7d）刺激rCFs激活Wnt/β-catenin通路，诱导小鼠心功能障碍和心肌纤维化[3]。