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多omics研究揭示了自相关蛋白质在自闭症谱系障碍中的差异表达和酸化
Eden Deri1, Shashank Kumar Ojha1, Maryam Kartawy1
1Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Scientific reports
|March 29, 2025
概括
自闭症谱系障碍 (ASD) 涉及被破坏的自,与改变的蛋白质酸化和氧化信号. 在ASD模型中抑制神经元氧化合成酶 (nNOS) 正常化的自标志物.
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 遗传学 是一个
背景情况:
- 自闭症谱系障碍 (ASD) 是一种复杂的神经发育状况,分子基础不明.
- 克3和Cntnap2基因突变与自闭症相关,使得克3Δ4-22和Cntnap2-/-小鼠模型对研究有价值.
研究的目的:
- 在ASD中使用Shank3Δ4-22和Cntnap2-/-小鼠模型调查共享的分子机制.
- 确定关键途径和受ASD影响的蛋白质,重点关注自和突触功能.
主要方法:
- 鼠类皮层的全球和蛋白学分析.
- 对SH-SY5Y细胞与SHANK3基因缺失和初级培养神经元的分析.
- 研究了氧化 (NO) 和神经元氧化合成酶 (nNOS) 在自失调中的作用.
主要成果:
- 在两个ASD小鼠模型中,自被显著影响,蛋白质表达和酸化发生改变.
- 像mTOR信号传递这样的关键通路受到影响,特定的自相关蛋白质 (ULK2,RB1CC1,ATG16L1,ATG9) 显示酸化发生改变.
- 细胞中的SHANK3缺失表明自细胞-溶酶体融合受损,氧化信号与自细胞失调有关.
- 在细胞和神经元模型中,通过7-NI正常化的自标记物抑制nNOS.
结论:
- 多omics数据揭示了自相关蛋白质在ASD中的差异性表达和酸化.
- 氧化信号干扰有助于ASD的自功能受损.
- 抑制nNOS是一种潜在的治疗策略,可以在ASD中使自细胞正常化,因此需要进一步研究已识别的酸化部位.
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