The study of the molecular mechanism of polyglutamine disease model mice and search for new therapeutic molecule

利用扩增的155只多聚谷氨酰胺高表达转基因小鼠，通过序贯免疫印迹分析和免疫荧光研究，分析了小鼠从临床病程早期到病程结束的分子机制。我们发现，高尔基体的碎裂发生在TG小鼠的早期。此外，我们还发现其中一个高尔基体相关分子的蛋白表达水平升高，并且定位与早期的产仔小鼠不同。

Using the expanded 155 polyglutamine overexpression transgenic mice, we analyzed the molecular mechanism of the mice from the early to end stage of the clinical course by sequential western blot analysis and immunofluorescence study. We revealed that the fragmentation of Golgi apparatus were occurred in early stage of the Tg mice. Further, we identified one of the Golgi related molecule was increased in protein expression level and the localization was different compared to the littermate NT mice at early stage.