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Caffeic acid phenethyl ester accumulates beta-catenin through GSK-3beta and participates in proliferation through mTOR in C2C12 cells

机译:咖啡酸苯乙烷通过GSK-3Beta积累β-连环蛋白,并通过C2C12细胞中的MTOR参与增殖

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Aim: The aim of this study is to characterize the roles of caffeic acid phenethyl ester (CAPE) in the skeletal muscle cells.Main methods." We performed immunoblotting assay using various phosphorylation specific antibodies. Key findings: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3beta in a phosphoinositide 3-kinase (PI3K)-dependent manner. CAPE also decreases phosphorylation of beta-catenin, ultimately leading to beta-catenin accumulation. In addition, we demonstrated that CAPE activated the mammalian target of rapamycin (mTOR)-p70 S6 ribosomal kinase (S6K) and also stimulated extracellular signal-regulated kinase (ERK). The inhibition of mTOR blocked CAPE-induced ERK phosphorylation.Significance: Our results suggest that CAPE may act through beta-catenin accumulation via stimulation of GSK-3beta and may also participate in cellular proliferation through the mTOR-ERK pathway.
机译:目的:本研究的目的是表征咖啡酸苯乙烷酯(辣椒)在骨骼肌细胞中的作用。“我们使用各种磷酸化特异性抗体进行免疫印迹测定。关键发现:我们发现斗篷突然迅速诱导 磷酸阳性3-激酶(PI3K)依赖性糖苷合成酶激酶(GSK)-3β的瞬时磷酸化。己酸还原β-catenin的磷酸化,最终导致β-catenin积累。此外,我们证明了斗篷激活了 哺乳动物雷帕霉素(MTOR)-P70 S6核糖体激酶(S6K)的靶标和刺激的细胞外信号调节激酶(ERK)。MTOR被封闭的海角诱导的ERK磷酸化。我们的结果表明披风可以通过β- 通过刺激GSK-3Beta的Catenin积累,并且还可以通过MTOR-ERK途径参与细胞增殖。

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