纤维素C通过焦点粘附周转和动氨酸稳定调节细胞机制响应
E S Klimenko1, M Yu Sorokina1, K S Sukhareva1
1Almazov National Medical Research Centre, Saint-Petersburg, Russia.
Cytoskeleton (Hoboken, N.J.)
|February 22, 2026
概括
纤维素C缺乏会破坏肌肉细胞的分化,因为它会破坏焦点粘附周转和actomyosin稳定,从而损害YAP/TAZ和β-catenin信号通路.
科学领域:
- 细胞生物学 细胞生物学
- 肌肉的发展 肌肉的发展
- 机械转导是指机械转导的过程.
背景情况:
- 纤维素C (FLNC) 对于细胞骨完整性和机械感知至关重要.
- 功能障碍的机械敏感通道,包括YAP/TAZ和β-catenin,与各种肌肉疾病有关.
- FLNC在调节这些通路中的确切作用尚不清楚.
研究的目的:
- 为了研究纤维素C缺乏细胞中受损的YAP/TAZ和β-catenin信号传递的机制基础.
- 阐明 C 纤维素在调节行为体细胞骨组织,焦点粘附动力学和机械传导中的作用.
主要方法:
- 使用的胺C淘汰 (FlncKO) C2C12细胞核细胞.
- 分析了转录组形状,actin组织和焦点粘附结构.
- 使用药理抑制剂 (维特波芬,贾斯普拉基诺利德, (-) 布莱比斯塔丁,Y-27632) 来探测信号通路.
主要成果:
- 纤维素C缺乏导致F/G-actin比率增加,焦点粘附增加,核YAP/TAZ和β-catenin减少.
- 动蛋白稳定 (Jasplakinolide) 挽救了FlncKO细胞中的YAP/TAZ信号传递.
- ROCK抑制 (Y-27632) 促进了焦点粘附分解,并恢复了β-catenin局部化,特别是在FlncKO细胞中.
结论:
- 纤维素C对于正确的焦点粘附周转和C2C12肌肉细胞中actomyosin复合物的稳定是必不可少的.
- 缺乏FLNC会影响YAP/TAZ和β-catenin的机械传导,影响肌肉细胞在肌芽细胞阶段的分化.
- 针对异常的焦点粘附动态可能为FLNC相关的肌肉病变提供治疗策略.
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