机译:PKB信号传导的破坏恢复极性对缺乏肿瘤抑制器PTEN的细胞
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
Department of Cell Biology School of Medicine Johns Hopkins University Baltimore MD 21205;
PakA; p21-activated kinase A; PDK; phosphoinositide-dependent protein kinase; PIP_3; phosphotidylinositol 3; 4; 5-triphosphate; PI3K; phosphoinositide 3-kinase; PKB; protein kinase B; PLA_2; phospholipase A_2; PTEN; phosphatase and tensin homologue; TORC2; target of rapamycin complex 2;
机译:PKB信号的破坏可恢复缺乏肿瘤抑制因子PTEN的细胞的极性
机译:胶质母细胞瘤细胞中的蛋白激酶B(PKB / Akt)活性由于肿瘤抑制因子PTEN / MMAC的突变而升高
机译:抑癌基因PTEN通过PKB和FAK共同影响人肺癌细胞凋亡
机译:肿瘤抑制基因PTEN在前列腺癌细胞系中的细胞周期调节和细胞凋亡中起着作用
机译:FGFR信号传导和肿瘤抑制因子TSC和PTEN调节果蝇血液祖细胞的生长和分化
机译:PKB信号的破坏可恢复缺乏肿瘤抑制因子PTEN的细胞的极性
机译:PKB信号的破坏可恢复缺乏肿瘤抑制因子PTEN的细胞的极性
机译:通过重建肿瘤抑制因子pTEN恢复对前列腺癌细胞凋亡的敏感性