14-3-3蛋白在环境毒物鱼藤酮诱导多巴胺神经元α-synuclein核转位的作用和机制研究
基本信息
结项摘要
α-synuclein功能异常是鱼藤酮诱发帕金森病样症状的主要原因 。鱼藤酮注射大鼠多巴胺神经元核内出现α-synuclein表达。α-synuclein核转位可能参与鱼藤酮多巴胺神经元的退变作用。目前α-synuclein核转位的作用和机制不明。14-3-3蛋白可通过调节靶蛋白与其他结合蛋白之间或两个靶蛋白之间的相互作用，调节靶蛋白的核浆转运。14-3-3蛋白和α-synuclein的复合体参与Parkinson病的发病。因此，本课题建立鱼藤酮染毒SH-SY5Y模型，观察鱼藤酮诱导α-synuclein核转位及其与DNA和组蛋白的作用；研究14-3-3蛋白在α-synuclein核转位中的作用；探讨14-3-3蛋白参与α-synuclein核转位的作用机制。以揭示多巴胺神经元中α-synuclein核转位的机制和探讨α-synuclein在鱼藤酮多巴胺神经元损伤中的作用。
项目摘要
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数据更新时间：2023-05-31
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