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首页> 外文期刊>Cellular immunology >ICBP90 mediates the ERK1/2 signaling to regulate the proliferation of Jurkat T cells.
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ICBP90 mediates the ERK1/2 signaling to regulate the proliferation of Jurkat T cells.

机译：ICBP90介导ERK1 / 2信号调节Jurkat T细胞的增殖。

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摘要

ERK1/2 activation leads to the release of E2F that could bind to the E2F binding sites in the inverted CCAAT box binding protein (ICBP90) gene promoter. Therefore, in the present study the relationship between ERK1/2 signaling and ICBP90 in the regulation of Jurkat T cell proliferation was explored. Jurkat T cells were treated with different concentrations of various signal pathway inhibitors. The cell viability and cell cycle were determined. Furthermore, the expression of non-phosphorylated and phosphorylated ERK1/2, and ICBP90 was measured by Western blot analysis. All the inhibitors, including PD98059, LY294002, AG490, genistein and GF109203X, suppressed the cell colony formation and proliferation to different extent in a dose-dependent manner. PD98059 could suppress the cell proliferation remarkably, arrested the cell cycle at G1/G0 stage and blocked its entrance from S phase to G2/M phase. Three or 24h after exposure to the inhibitors, all the inhibitors downregulated the level of the phosphorylated ERK1/2, of which the inhibitory roles of PD98059, LY294002 and AG490 were more significant. All the inhibitors had no effect on the expression of ICBP90 after 3h treatment, but downregulated markedly its expression after 24h treatment, especially PD98059, LY294002 and AG490. The expression of ICBP90 was directly proportioned to the level of ERK1/2 phosphorylation and the cell proliferation. Our results demonstrate that ICBP90 might be a pivotal target for the ERK1/2 signaling pathway to control the proliferation of Jurkat T cells.
机译：ERK1 / 2激活导致E2F释放，该E2F可能与反向CCAAT盒结合蛋白（ICBP90）基因启动子中的E2F结合位点结合。因此，在本研究中，探索了ERK1 / 2信号传导和ICBP90在Jurkat T细胞增殖调控中的关系。用不同浓度的各种信号途径抑制剂处理Jurkat T细胞。测定细胞活力和细胞周期。此外，通过蛋白质印迹分析测量了非磷酸化和磷酸化的ERK1 / 2和ICBP90的表达。所有抑制剂，包括PD98059，LY294002，AG490，染料木黄酮和GF109203X，均以剂量依赖性方式抑制细胞集落的形成和增殖。 PD98059能显着抑制细胞增殖，使细胞周期停在G1 / G0期，阻止其从S期进入G2 / M期。暴露于抑制剂后3或24小时，所有抑制剂均下调磷酸化ERK1 / 2的水平，其中PD98059，LY294002和AG490的抑制作用更为显着。 3h处理后所有抑制剂对ICBP90的表达均无影响，但24h处理后其表达明显下调，尤其是PD98059，LY294002和AG490。 ICBP90的表达与ERK1 / 2磷酸化水平和细胞增殖成正比。我们的结果表明，ICBP90可能是ERK1 / 2信号通路控制Jurkat T细胞增殖的关键靶标。

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