ATF3调控神经元凋亡的作用及其机制
基本信息
结项摘要
我们首次报道了撤钾诱导的内源性ATF3促神经元凋亡；同时我们和其他实验室也发现过表达ATF3抑制凋亡。这表明内源性ATF3和过表达ATF3对神经元凋亡的作用不同，但其机制仍不清楚。预实验结果表明：内源性ATF3与c-Jun形成二聚体；过表达ATF3与MLK3相互作用且抑制了MLK3下游激酶JNK的底物c-Jun和ATF2的活性。由此，我们提出ATF3调控神经元凋亡的新机制，即：内源性ATF3与c-Jun形成二聚体发挥促凋亡作用；过表达ATF3抑制JNK上游激酶MLK3的活性从而保护性干预凋亡。本项目拟进一步采用BiFC、siRNA、CoIP、腺病毒表达等方法，获得ATF3以不同的机制发挥相应作用的可靠证据；旨在揭示ATF3调控神经元凋亡的本质、为确立ATF3作为神经退行性疾病治疗的新靶点提供更充分的科学依据。
项目摘要
项目成果
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数据更新时间：2023-05-31
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