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机译:蜗牛通过PI3K / AKT依赖的RAC1激活以及在前列腺癌进展期间的PI3K / AKT无关的途径促进细胞迁移
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
Center for Cancer Research and Therapeutic Development;
Department of Biological Sciences;
Clark;
cell migration; MAPK pathway; PI3K/AKT pathway; Rac1; snail;
机译:蜗牛在前列腺癌进展过程中通过PI3K / AKT依赖性Rac1激活以及PI3K / AKT依赖性途径促进细胞迁移
机译:花生四烯酸通过PI3K / Akt依赖性途径促进MDA-MB-231乳腺癌细胞的迁移和侵袭
机译:层粘蛋白A / C蛋白在组织侵袭性前列腺癌中过表达,并通过PI3K / AKT / PTEN途径促进前列腺癌细胞的生长,迁移和侵袭
机译:PI3K途径在抗IgM(抗IgM(抗-Ig)的作用 - 最终和 - 抗生素B细胞淋巴瘤未脱离PI3K途径信号传导对CH12 B细胞淋巴瘤的I-FI阻力
机译:多靶点受体酪氨酸激酶抑制剂利尼法尼(ABT-869)通过磷酸肌醇3激酶(PI3K)/ AKT依赖性信号传导途径诱导凋亡并抑制白血病细胞的增殖。
机译:蜗牛在前列腺癌进展过程中通过PI3K / AKT依赖性Rac1激活以及PI3K / AKT依赖性途径促进细胞迁移
机译:蜗牛通过PI3K / AKT依赖的RAC1激活促进细胞迁移,以及前列腺癌进展期间的PI3K / AKT无关的途径
机译:分子靶向pI3K / akt通路预防激素抵抗前列腺癌的发生