机译:IL-17A通过SRC / MAPK / PI3K / NF-KB途径诱导原代星形胶质细胞的MIP-1α表达:对多发性硬化症的影响(Vol 9,PG 629,2014)
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
Univ Nebraska Med Ctr Dept Pharmacol &
Expt Neurosci Omaha NE USA;
Nanjing Univ Jinling Hosp Med Sch Dept Urol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Physiol Nanjing Peoples R China;
Southeast Univ Med Sch Dept Pharmacol Nanjing Peoples R China;
机译:IL-17A通过Src / MAPK / PI3K / NF-kB途径诱导原代星形胶质细胞MIP-1 alpha表达:对多发性硬化症的影响
机译:日本脑炎病毒通过ROS / c-Src / PDGFR / PI3K / Akt / MAPKs依赖性AP-1途径在大鼠脑星形胶质细胞中诱导基质金属蛋白酶9表达
机译:巨噬细胞炎性蛋白1α(MIP-1 alpha)通过MAPK和PI3K / Akt途径增强小鼠骨髓基质细胞和成骨细胞中核因子kappa B配体(RANKL)表达的受体激活剂
机译:Fractalkine诱导CD4 + T淋巴细胞上细胞间粘附分子1的表达:对多发性硬化症的免疫发病机制的意义
机译:日本脑炎病毒通过ROS / c-Src / PDGFR / PI3K / Akt / MAPKs依赖性AP-1途径在大鼠脑星形胶质细胞中诱导基质金属蛋白酶9表达
机译:校正至:IL-17A通过SRC / MAPK / PI3K / NF-KB途径诱导原代星形胶质细胞中的MIP-1α表达:对多发性硬化的影响