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非磷酸化的CREB和ERK没有显著变化。The total ERK and CREB had no significant changes.

免疫组织化学显示ERK蛋白主要位于细胞浆内。Immunohistochemistry showed that ERK protein were mainly located in cytoplasm.

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氨甲酰胆碱对神经元的保护作用及对ERK激活的抑制作用可被阿托品阻断。The protective effect and the inhibiting ERK phosphorylation of carbachol were blocked by atropine.

免疫印迹结果表明凝集素激活了B淋巴细胞的ERK通路,促进了B淋巴细胞的增殖。Results of western blotting showed that ERK signaling pathway in B lymphocytes proliferation was activated by MPL.

由此我们推测,低氧引起ECV304细胞分泌VEGF增加有可能是通过ERK和P38通路来介导。These results suggest that hypoxia-induced VEGF up-regulation is mediated by ERK and P38 kinases pathways in ECV304 cells.

结论蛋白酪氨酸激酶、HER2激酶、ERK激酶和PDGFR激酶途径是胃癌细胞抗脱落凋亡的重要信号通路和信号分子。Conclusions Protein tyrosine kinase, HER2 kinase, ERK kinase and PDGFR kinase pathway are important signal molecule and signal pathway.

方法应用免疫组织化学方法检测ERK在脊髓后角的定位表达,并用图像分析系统和免疫印迹法进行定量分析。Methods The expression of ERK in spinal dorsal horn was detected by immunohistochemical method and was quantitated by western-blot analyses.

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更重要的是,信号通路研究显示ERK的磷酸化可以被Y356F突变完全阻断或者被Y327F突变显著降低。Importantly, signaling studies revealed that the activation of ERK pathway was completely inhibited by Y356F and significantly reduced by Y327F.

尾吊诱发的模拟失重效应可能通过抑制ERK在大鼠股动脉粗、细肌丝调节中的作用从而损伤其收缩反应。Simulated microgravity may attenuate the contractile responses of femoral arteries by inhibiting the ERK in thick and thin filament regulatory pathways.

结论D1和D3多巴胺受体对CREB的磷酸化活化起反式调控作用,并且这种反式调控作用依赖于ERK信号通路。Conclusion D1 and D3 dopamine receptors can oppositely regulate CREB activation after cocaine treatment and this regulation depends on ERK signaling pathway.

结论对离体培养的人大隐静脉平滑肌细胞磷酸化ERK进行阻断后,平滑肌细胞的增殖受抑,凋亡增加,细胞由合成型向收缩型转变。Conclusion After the activated ERK was inhibited, the degree of cellular proliferation was decreased, the degree of apoptosis increased and the phenotype changed from synthetic to contractile.