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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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基础科学和病原发生学

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删除tau的N和C末端会产生模仿阿尔茨海默病病理学的tau聚合物. 这些截断的聚合物在细胞和小鼠大脑中促进了进一步的聚和高酸化.

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科学领域:

  • 神经科学是一个神经科学.
  • 生物化学 生物化学
  • 病理学 病理学 病理学

背景情况:

  • 由高酸化组成的神经纤维状 (NFT) 是阿尔茨海默病 (AD) 的关键.
  • 陶氏病理通过类似子的机制传播,起源于特定的大脑区域,并随着时间的推移而进展.
  • 在阿尔茨海默氏病中,丧失了N和C末端,可能导致自我聚合和疾病进展.

研究的目的:

  • 调查结末删除在聚和蛋白质治疗性质中的作用.
  • 为了确定切断的是否可以在体外和体内诱导病理.

主要方法:

  • 产生了一个缺少N-和C-末端的截断的tau蛋白 (tau151-391).
  • 使用超离心法诱导的陶聚合,在HEK-293T细胞中过度表达.
  • 评估了酸化和蛋白质治疗性质在体外和体内.

主要成果:

  • 截断的 (tau151-391) 在细胞和小鼠大脑中形成聚合物,与全长的不同.
  • 聚合的tau151-391是高酸化的,并且部分抵抗蛋白酶K消化.
  • 陶151-391聚合物在细胞和小鼠大脑中诱导了进一步的陶聚合和高酸化.

结论:

  • 淘的N-和C-末端的删除促进聚合,并赋予蛋白质治疗特征.
  • 陶151-391聚合物是陶聚合和特定位点过酸化的强有力的诱导剂.