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机译:LINC00152敲除灭活AKT / MTOR和Notch1途径,以发挥其抗血管瘤效应
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Henan Prov Peoples Hosp Dept Hemangioma &
Vasc Malformat 7 Weiwu Rd Zhengzhou 450003 Henan;
Infantile hemangioma; Long non-coding RNAs; Hemangioma-derived endothelial cells; Linc00152; Akt/mTOR; Notch1;
机译:LINC00152敲除灭活AKT / MTOR和Notch1途径,以发挥其抗血管瘤效应
机译:LNCRNA LINC00152敲低的效果抑制肺癌的生物活性通过EGFR / PI3K / AKT途径
机译:分化抑制剂1抑制抑制增殖并通过在血管瘤衍生的内皮细胞中灭活PI3K / AKT / mT信号传导来诱导细胞凋亡
机译:多重免疫沉淀和靶向质谱法的定量分析AKT / mTOR途径
机译:Akt和JNK途径的双重调节剂靶向人类腺癌细胞中的mTOR
机译:敲低lncRNA XIST可通过使miR-375-3p失活而使AKT / mTOR信号通路失活而抑制骨肉瘤的进展
机译:骨桥蛋白抑制抑制αv,β3整合素诱导的细胞迁移和侵袭,并通过诱导自噬和灭活pI3K / akt / mTOR途径促进乳腺癌细胞的凋亡