• So the study of PI3K-Akt maybe a new target in searching drug treatment of tumor.

    因此,通过对PI3K通路的研究有望寻求肿瘤药物治疗的新靶点。

    youdao

  • AKT inhibitors have been used in trials on cancer patients before but with limited success.

    AKT抑制剂以前在癌症患者身上做过实验,但效果有限。

    youdao

  • "This underscores the importance of discovering the origin of active Akt in glioblastomas," he said.

    “这突出了发现胶质母细胞瘤中活性Akt蛋白的重要性,”他说。

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  • Decreased PTEN protein and increased AKT protein might be a marker for the early detection of the occurrence of colorectal cancer in patients with UC.

    PTEN蛋白表达的明显降低和AKT蛋白表达的明显增强有可能成为早期监测uc癌变的一个辅助指标。

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  • This data complements Drosophila genetics studies suggesting the possible involvement of the tuberin-hamartin complex in the PI3K/Akt mediated insulin pathway (8-10).

    这些数据和果蝇(Drosophila)遗传学研究表明tuberin-hamartin 复合物可能在PI3K/AKT介导的胰岛素通路中取作用(8-10)。

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  • Conclusion: ROS, PTEN and p-AKT are involved in the signaling pathway of glucose-stimulated insulin secretion in INS-1cell, as signaling molecules in insulin secretion.

    结论:ROS、PTEN及P -AKT参与了葡萄糖刺激INS - 1细胞分泌胰岛素的信号通路,成为介导胰岛素分泌的信号分子。

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  • Zakrzewicz will present data from studies showing that the transcription factor Foxo-1, first described in 1999, can be inactivated by shear stress via Akt-mediated phosphorylation.

    Zakrzewicz在他的综述中所提供的研究数据表明Foxo - 1转录因子(1999年首次被描述)可以被剪切应力通过Akt所介导的磷酸化作用所灭活。

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  • The AKT-mediated signal pathway has been shown to be impaired in patients with schizophrenia, and antipsychotic medication may induce AKT activation, to compensate for the impairment.

    AKT介导的信号通路在精神分裂症患者中发现有受损,而抗精神分裂症药物可以导致AKT激活,补偿这种受损。

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  • Aim: To investigate the expression of phosphorylated AKT (p-AKT) and proliferating cell nuclear antigen (PCNA) in human non-small cell lung cancer (NSCLC) tissue and their correlations.

    目的探讨非小细胞肺癌(NSCLC)组织中磷酸化akt (p -AKT)和细胞增殖核抗原(pcna)的表达。

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  • A recent clinical trial using an EGFR inhibitor found that patients whose tumors expressed high levels of phosphorylated - or chemically altered - Akt did not respond to treatment, Kwatra said.

    最近一项使用表皮生长因子受体抑制剂的临床试验发现,患者的肿瘤细胞表达磷酸化或化学转化水平很高-Akt对这种疗法没有反应“Kwatra博士说。”

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  • We propose that the elevated levels of phosphorylated Akt may come from active forms of NK1R, and it's possible that a better response might be obtained by simultaneously blocking EGFR and NK1R.

    我们预测高浓度的磷酸化akt蛋白可能来自活化的NK1R受体,所以同时抑制EGFR和NK1R受体可能获得更好的效果。

    youdao

  • We propose that the elevated levels of phosphorylated Akt may come from active forms of NK1R, and it's possible that a better response might be obtained by simultaneously blocking EGFR and NK1R.

    我们预测高浓度的磷酸化akt蛋白可能来自活化的NK1R受体,所以同时抑制EGFR和NK1R受体可能获得更好的效果。

    youdao

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