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机译:MicroRNA-139-5P通过与IGF1R结合,通过PI3K / AKT信号通路调节恶性黑素瘤细胞的生长和转移
Sun Yat SenUniv Affiliated Hosp 6 Dept Dermatol Guangzhou Peoples R China;
Sun Yat SenUniv Affiliated Hosp 6 Dept Ophthalmol Guangzhou Peoples R China;
Sun Yat SenUniv Affiliated Hosp 6 Dept Dermatol Guangzhou Peoples R China;
Sun Yat SenUniv Affiliated Hosp 6 Dept Dermatol Guangzhou Peoples R China;
Sun Yat SenUniv Affiliated Hosp 6 Dept Dermatol Guangzhou Peoples R China;
Shanghai Jiao Tong Univ Xinhua Hosp Sch Med Dept Dermatol Shanghai Peoples R China;
Sun Yat SenUniv Affiliated Hosp 6 Dept Dermatol Guangzhou Peoples R China;
MicroRNA-139-5p; IGF1R; PI3K/AKT signaling pathway;
机译:MicroRNA-139-5P通过与IGF1R结合(Vol 18,PG 3513,2020)通过PI3K / AKT信号传导途径调节恶性黑素瘤细胞的生长和转移
机译:MicroRNA-153-3P抑制视网膜母细胞瘤细胞生长和侵袭通过靶向IGF1R / RAF / MEK和IGF1R / PI3K / AKT信号通路
机译:G蛋白信号调节剂2在肝细胞癌中的高表达通过激活PI3K / AKT信号通路促进肿瘤生长和转移
机译:E3泛素连接酶CBL-B通过抑制PI3K / AKT信号通路和P-糖蛋白下调逆转MCF-7 / ADR细胞的多药耐药性
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:MicroRNA-139-5P通过与IGF1R结合通过PI3K / AKT信号通路调节恶性黑素瘤细胞的生长和转移
机译:MicroRNA-139-5P通过与IGF1R结合,通过PI3K / AKT信号通路调节恶性黑素瘤细胞的生长和转移