机译:微囊藻毒素-LR引起的ROS生成涉及神经内分泌(PC12)细胞中的p38激活和Tau过度磷酸化。
Department of Clinical Laboratory, Tongde Hospital of Zhejiang Province, 234 Gucui Road, Hangzhou 310012, China,Department of Biochemistry, School of Medicine, Zhejiang University, 866th Yu Hang Tang Road, Hangzhou 310058, China;
Department of Biochemistry, School of Medicine, Zhejiang University, 866th Yu Hang Tang Road, Hangzhou 310058, China;
Department of Biochemistry, School of Medicine, Zhejiang University, 866th Yu Hang Tang Road, Hangzhou 310058, China;
Department of Biosystem Engineering, College of Biosystem Engineering and Food Science, 866th Yu Hang Tang Road, Hangzhou 310058, China;
Department of Biochemistry, School of Medicine, Zhejiang University, 866th Yu Hang Tang Road, Hangzhou 310058, China;
microcystin-LR; reactive oxygen species; tau hyperphosphorylation; p38 mitogen-activated protein kinase;
机译:微囊藻毒素-LR通过PP2A抑制tau和HSP27的过度磷酸化以及随后激活神经内分泌(PC12)细胞中的p38 MAPK信号通路而诱导细胞骨架系统重组。
机译:微囊杆菌-LR通过PP2A抑制和随后的P38 MAPK信号通路在神经内分泌(PC12)细胞中的P38 MAPK信号通路的激活来诱导细胞骨架系统重组。
机译:更正:锰通过激活PC12细胞中ERK MAPK途径诱导tau蛋白过度磷酸化
机译:中度白噪声引起的海马Tau过度磷酸化引起的过氧化损伤
机译:使用CRISPR-Cas 9去除PC12神经内分泌细胞中野生型VHL肿瘤抑制基因的作用
机译:ROS激活的p38MAPK途径的抑制作用涉及H2S对PC12细胞化学性低氧诱导的炎症的保护作用。
机译:锰通过在PC12细胞中激活ERK MAPK途径诱导TAU高磷酸化