机译:EPOTHILONE D在肌营养侧面硬化症的SOD1 G93A G93A模型中加速疾病进展
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Florey Institute of Neuroscience and Mental HealthParkville Vic. Australia;
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Menzies Institute for Medical ResearchUniversity of TasmaniaHobart Tas. Australia;
Amyotrophic Lateral Sclerosis; Epothilone D; Microtubule stabilisation; Toxicity; Motor behaviour; Microtubules;
机译:EPOTHILONE D在肌营养侧面硬化症的SOD1 G93A G93A模型中加速疾病进展
机译:等体内遗传烧蚀的代谢谷氨酸受体类型5减慢了肌营养侧硬化症的SOD1(G93A)小鼠模型中的疾病进展
机译:肌萎缩性侧索硬化症的SOD1 G93A小鼠模型中遗传背景和性别对疾病进展的贡献的Meta分析
机译:MARDI-TOF MS和FT-ICR MS的家族性肌萎缩外硬化相关交联Cu,Zn超氧化物歧化酶(SOD1)的分析
机译:肌萎缩性侧索硬化的小鼠模型中G93A HSOD1转基因复合物的表征。
机译:在肌萎缩性侧索硬化症的SOD1 G93A小鼠模型中,在疾病进展过程中星形胶质细胞的溶酶体和吞噬活性增加
机译:缺失Galectin-3加剧了显微胶质激活并加速疾病进展,并在肌营养的侧面硬化症的SOD1 G93A小鼠模型中进行消亡