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机译:IFN-γ介导的肺癌抑制与PD-L1表达相关,并通过PI3K-AKT信号调节
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
Department of Thoracic SurgeryTongji Hospital Tongji Medical College Huazhong University of;
IFNG; PD‐L1; PI3K; STAT1; lung adenocarcinoma;
机译:IFN-γ介导的肺癌抑制与PD-L1表达相关,并通过PI3K-AKT信号调节
机译:MiR-205的抑制序列通过调节PETN介导的PI3K / AKT信号途径阻碍了细胞增殖和肺癌细胞迁移
机译:来自肿瘤相关巨噬细胞的IFN-γ引起的PD-L1通过JAK / Stat3和PI3K / AKT信号通路促进了肺癌的进展
机译:半胱氨酸天冬氨酸蛋白酶激活和细胞外信号调节激酶/ Akt抑制涉及路易斯-肺癌细胞中木犀草素诱导的细胞凋亡。
机译:FGF8通过MEK / ERK和PI3K / AKT信号转导级联调节新皮质原基中的模式和基因表达。
机译:PD‐L1通过维持PI3K / AKT途径活化来促进乳腺癌干细胞中的OCT4和Nanog表达
机译:ILT4通过PI3K / AKT / mTOR信号传导驱动B7-H3表达,ILT4 / B7-H3共表达与非小细胞肺癌预后不良相关
机译:IL-1和肿瘤坏死因子-α各自上调IFN-γ受体的表达并增强人单核细胞和人单核细胞系(THp-1)上IFN-γ诱导的HLa-DR表达