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Role of extracellular signal-regulated kinase 1/2 signal transduction pathway in insulin secretion by beta-TC6 cells

机译:细胞外信号调节激酶1/2信号转导通路在β-TC6细胞分泌胰岛素中的作用

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The present study aimed to investigate the role of the extracellular signal-regulated kinase (ERK) 1/2 signal transduction pathway in glucose-stimulated insulin secretion in beta-TC6 mouse pancreatic cells. Insulin production by beta-TC6 cells was stimulated with various concentrations of glucose, which was dose-dependently inhibited by mitogen-activated protein kinase inhibitor PD98059, as indicated by a radioimmunoassay. Furthermore, glucose stimulation enhanced the phosphorylation of ERK1/2, which was dose-dependently inhibited by PD98059, as indicated by western blot analysis. These results indicated that the activation of the ERK1/2 signal transduction pathway may have an important role in glucose-stimulated insulin secretion in beta-TC6 cells.
机译:本研究旨在调查细胞外信号调节激酶(ERK)1/2信号转导通路在β-TC6小鼠胰腺细胞中葡萄糖刺激的胰岛素分泌中的作用。如放射免疫分析所示,用各种浓度的葡萄糖刺激β-TC6细胞产生的胰岛素,该剂量被促分裂原活化的蛋白激酶抑制剂PD98059剂量依赖性地抑制。此外,如蛋白印迹分析所示,葡萄糖刺激增强了ERK1 / 2的磷酸化,PD98059剂量依赖性地抑制了ERK1 / 2的磷酸化。这些结果表明ERK1 / 2信号转导途径的激活可能在β-TC6细胞中葡萄糖刺激的胰岛素分泌中起重要作用。

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