机译:IGFBP-5诱导的纤维化表型受MAPK激活和Egr-1依赖性和非依赖性机制的调节。
From the Division of Pulmonary, Allergy, and Critical Care Medicine,Boston, Massachusetts;
From the Division of Pulmonary, Allergy, and Critical Care Medicine,Boston, Massachusetts;
From the Division of Pulmonary, Allergy, and Critical Care Medicine,Boston, Massachusetts;
the Division of Hematology and Oncology,Boston, Massachusetts;
University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, and Brigham and Women’s Hospital,Boston, Massachusetts;
From the Division of Pulmonary, Allergy, and Critical Care Medicine,Boston, Massachusetts|Department of Medicine, and the Department of Pathology,Boston, Massachusetts;
机译:IGFBP-5诱导的纤维化表型受MAPK激活以及egr-1依赖性和非依赖性机制调节。
机译:细胞因子诱导的白细胞介素-8的下调需要通过MAPK磷酸酶1依赖性和依赖性机制抑制P38丝裂原活化蛋白激酶(MAPK)
机译:Evodiamine以一种不依赖蛋白1的方式改善饮食诱导的肥胖:参与抗脂肪形成机制和细胞外调节的激酶/促分裂原激活的蛋白激酶信号传导。
机译:氧化铁纳米颗粒通过调节NF-kB和MAPK信号通路抑制RANKL诱导的破骨细胞生成
机译:肾脏损伤过程中蛋白磷酸酶镁依赖性1A(PPM1A)放松促进通过SMAD3-PAI-1依赖性机制的纤维化表型。
机译:IGFBP-5诱导的纤维化表型受MAPK激活和Egr-1依赖性和非依赖性机制的调节。
机译:IGFBP-5诱导的纤维化表型受MAPK激活和Egr-1依赖性和非依赖性机制的调节。
机译:mapK诱导产生ER阴性表型的下游信号机制