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通过MARCHF7/MARCH7介导的全方位化来控制ATG14溶解度和自
Xue Shi1,2, Xiaofei Zhang1,2
1Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong, China.
Autophagy
|November 2, 2023
概括
通过促进蛋白质聚合,ATG14的MARCHF7蛋白质泛基化会损害自流. MARCHF7淘汰会减少类似攻击性的结构,这表明神经退行性疾病的治疗潜力.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 翻译后修饰 (PTMs) 调节蛋白质功能,影响细胞过程,如自.
- 作为一个关键的PTM,ubiquitination控制着蛋白质的稳定性,活性和局部化.
- 自对于细胞平衡和降解受损组件至关重要.
研究的目的:
- 调查MARCHF7在ATG14无化中的作用及其对自的影响.
- 探索这种调节机制对蛋白质聚合物的降解的影响.
主要方法:
- 通过MARCHF7.7诱导的ATG14无处不在模式的分析.
- 评估ATG14的聚合和与STX17的相互作用.
- 在MARCHF7绝杀细胞中评估自流量.
- 攻击类诱导结构 (ALISs) 的量化.
主要成果:
- MARCHF7通过K6,K11和K63链接促进ATG14的混合多基化.
- 这种无处不在导致ATG14不溶性聚合和减少STX17相互作用.
- 自流量由于MARCHF7-介导的ATG14修饰而减少.
- 在MARCHF7的淘汰细胞中,ALIS的数量显著减少,这表明总体清除增强.
结论:
- ATG14的MARCHF7依赖的无处不在是一种新型的调节机制,会损害自.
- 这一途径有助于蛋白质聚合物的积累.
- 向MARCHF7可能为与蛋白质聚合和自功能受损相关的神经退行性疾病提供治疗策略.
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