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在帕金森病模型中,依赖Cdk5酸化的C9orf72降解促进神经元死亡

Xingfeng Xu^1,2, Mao Li^1,2, Yan Su^1,2

¹Department of Physiology, Guilin Medical University, Guilin, Guangxi, China.

CNS neuroscience & therapeutics

|June 24, 2023

概括

染色体9开放阅读框架72 (C9orf72) 由于Cdk5的酸化和降解,帕金森病 (PD) 的蛋白质水平下降. 恢复C9orf72功能可以缓解PD模型中的神经元死亡和运动缺陷.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

染色体9开放阅读框架72 (C9orf72) 在帕金森病 (PD) 发病过程中的作用目前尚不清楚.
C9orf72与各种神经退行性疾病有关,突出显示其在神经疾病中的潜在意义.

研究的目的:

调查C9orf72在帕金森病的发病过程中的潜在机制.
探索C9orf72,Cdk5和PD中神经元死亡之间的关系.

主要方法:

在PD模型中使用西式涂抹,RT-PCR和免疫沉来检查C9orf72表达和酸化.
利用生物信息学来预测C9orf72上的Cdk5酸化位点,并测试了Cdk5抑制剂ROSCOVITINE.
构建了C9orf72敲击和过度表达模型,并使用来干扰Cdk5酸化.

主要成果:

C9orf72蛋白水平降低,而mRNA在PD模型中保持不变,酸化增加.
在Ser9中,Cdk5直接化C9orf72,通过ubiquitin-proteasome路径促进其降解.
C9orf72敲击加剧了PD症状,而过度表达和Cdk5酸化干扰缓解了神经元功能障碍和运动缺陷.

结论:

在帕金森病的进展过程中,C9orf72在调节神经元死亡方面发挥着至关重要的作用.
对C9orf72的Cdk5依赖性降解是导致PD病变的一个关键机制.
向C9orf72的Cdk5酸化可能为帕金森病提供治疗策略.

关键词:

C9orf7272 是一个很好的方法.帕金森病的疾病.循环素依赖的蛋白质激酶5 蛋白质的酸化是蛋白质的酸化.乌比奎丁-蛋白酶体通路

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