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首页> 外文期刊>Process Biochemistry >Effect of a fungal immunomodulatory protein from Ganoderma tsugae on cell cycle and interferon-gamma production through phosphatidylinositol 3-kinase signal pathway
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Effect of a fungal immunomodulatory protein from Ganoderma tsugae on cell cycle and interferon-gamma production through phosphatidylinositol 3-kinase signal pathway

机译:灵芝真菌免疫调节蛋白通过磷脂酰肌醇3-激酶信号途径对细胞周期和干扰素-γ产生的影响

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A fungal immunomodulatory protein (FIP-gts) was purified from Ganoderma tsugae. Recombinant FIP-gts was expressed as glutathione S-transferase fusion protein in E. coli. In this study, recombinant FIP-gts promoted cell cycle progression from G0/G1 to S phase and signaling pathways were investigated in human peripheral mononuclear cells (HPBMCs) by PI staining and flow cytometry. FlP-gts significantly induced cytokine interferon-gamma (IFN-γ) expression. Pre-treatment of cells with phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor LY294002 abolished FlP-gts, induced increase in S phase, and inhibited IFN-γ secretion. Akt, a downstream effector of PI 3-kinase was phosphorylated and activated by FIP-gts. Results show that FIP-gts is a potent activator in PBMC and its effects are mediated via cytokine regulation of PI 3-kinase.
机译:从灵芝中纯化出真菌免疫调节蛋白(FIP-gts)。重组FIP-gts在大肠杆菌中表达为谷胱甘肽S-转移酶融合蛋白。在这项研究中,重组FIP-gts促进了细胞周期从G0 / G1到S期的发展,并通过PI染色和流式细胞术研究了人外周血单个核细胞(HPBMC)的信号通路。 FlP-gts显着诱导细胞因子干扰素-γ(IFN-γ)的表达。用磷脂酰肌醇3-激酶(PI 3-激酶)抑制剂LY294002预处理细胞可消除FlP-gts,诱导S期增加,并抑制IFN-γ分泌。 PI 3-激酶的下游效应子Akt被磷酸化并被FIP-gts激活。结果表明,FIP-gts是PBMC中的有效激活剂,其作用是通过PI 3激酶的细胞因子调节介导的。

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