机译:磷脂酰肌醇的分子机制3-激酶(PI3K)/蛋白激酶B(AKT)信号传导途径介导的胃癌自噬
Ningbo Yinzhou Peoples Hosp Oncol Clin Dept Tradit Chinese Med TCM Ningbo 315000 Zhejiang Peoples R China;
Ningbo Yinzhou Peoples Hosp Dept Tumor Radiotherapy Ningbo 315000 Zhejiang Peoples R China;
Ningbo Yinzhou Peoples Hosp Dept Gastroenterol Ningbo 315000 Zhejiang Peoples R China;
Ningbo Yinzhou Peoples Hosp Dept Gastrointestinal Surg Ningbo 31500A Zhejiang Peoples R China;
Ningbo Yinzhou Peoples Hosp Dept Gastroenterol Ningbo 315000 Zhejiang Peoples R China;
Ningbo Yinzhou Peoples Hosp Dept Tumor Radiotherapy Ningbo 315000 Zhejiang Peoples R China;
LY294002; Akt; MKN-45; Autophagy;
机译:磷脂酰肌醇的分子机制3-激酶(PI3K)/蛋白激酶B(AKT)信号传导途径介导的胃癌自噬
机译:MiR-184通过调节磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)信号通路来抑制肥厚瘢痕
机译:MiR-223通过抑制磷酸酶和三素同源物(PTEN)/磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B(AKT)信号通路,促进平滑肌细胞增殖和动脉粥样硬化斑块形成
机译:阐明磷脂酰肌醇3-激酶/ Akt途径
机译:磷脂酰肌醇(PI)3-激酶/ Akt蛋白激酶信号通路在大鼠交感神经元存活中的作用
机译:敲低缺氧诱导因子1α(HIF-1α)促进自噬并抑制卵巢癌细胞中雷帕霉素(mTOR)信号通路的磷脂酰肌醇3-激酶(PI3K)/ AKT /哺乳动物靶标
机译:2-甲氧基雌二醇衰减磷脂酰肌醇3-激酶/ AKT途径介导的胃癌转移