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机译:MuSK重症肌无力的小鼠被动转移模型:破坏的MuSK信号导致突触失败
Physiology and Bosch Institute,University of Sydney,Sydney,New South Wales,Australia;
Physiology and Bosch Institute,University of Sydney,Sydney,New South Wales,Australia;
Physiology and Bosch Institute,University of Sydney,Sydney,New South Wales,Australia;
Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences,Liaoning Medical University,Jinzhou,China;
Department of Molecular Medicine,Concord Hospital,Sydney,New South Wales,Australia;
Physiology and Bosch Institute,University of Sydney,Sydney,New South Wales,Australia;
myasthenia gravis; neuromuscular junction; neuromuscular disease; musclespecific kinase; mouse models;
机译:MuSK抗体血清阳性(MuSK +)实验性自身免疫性重症肌无力(EAMG)中mTOR信号通路的肌肉特异性调节
机译:在MuSK重症肌无力小鼠模型中,肌肉特异性激酶的强迫表达减缓突触后乙酰胆碱受体的损失
机译:3,4-二氨基吡啶可改善MuSK抗体诱导的重症肌无力小鼠模型中的神经肌肉传递
机译:麝香Myasthenia的致病性IgG4亚类自身抗体
机译:肌肉特异性激酶(MUSK)引起的重症肌无力的小鼠模型,直接蛋白相互作用调节大电导(BK)钙激活钾通道的门控和转运
机译:MuSK重症肌无力IgG4破坏了LRP4与MuSK的相互作用但IgG4和IgG1-3均可分散预先形成的不依赖Agrin的AChR簇
机译:MuSK重症肌无力IgG4破坏了LRP4与MuSK的相互作用,但IgG4和IgG1-3均可分散预先形成的非凝集素依赖性AChR簇。