通过失败的整合素粘附强化,YAP调解了细胞亡.
Lidan Shi1, Elisabeth Nadjar-Boger1, Hamidreza Jafarinia2
1Department of Genetics and Developmental Biology, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 31096, Israel.
Cell reports
|February 23, 2024
概括
在软矩阵上的细胞亡是由Yes相关蛋白 (YAP) 信号驱动的. 由软矩阵相互作用触发的YAP转移到核中,诱导了编程细胞死亡,揭示了YAP在细胞命运中的新角色.
科学领域:
- 细胞生物学 细胞生物学
- 生物物理学的生物物理.
- 生物化学 生物化学
背景情况:
- 细胞外矩阵 (ECM) 刚性显著影响细胞命运决策,影响诸如增殖等过程.
- 虽然YES相关蛋白 (YAP) 在硬基质细胞增殖中的作用已经确立,但其在软基质细胞中诱导亡的功能仍然不清楚.
研究的目的:
- 阐明YAP调节亡的机制,以应对不同的细胞外矩阵刚性.
- 研究YAP酸化和局部化的作用,在软与硬矩阵上的细胞命运决定中介.
主要方法:
- 对在不同刚度的矩阵上培养的细胞中Y357残留物YAP局部化和酸化的分析.
- 调查actomyosin收缩性调节对YAP信号传递和细胞命运的影响.
- 显微镜和生物化学测试以评估细胞粘附动态和YAP的核转位.
主要成果:
- 在软矩阵上,YAP被招募到小粘附点上,在Y357酸化,并转移到核中,促进细胞亡.
- 相反,刚性矩阵在大型粘附中表现出较低的Y357酸化水平,与细胞增殖相关.
- 在软矩阵上减少了actomyosin收缩性,促进了粘附生长,降低了Y357酸化,并促进了细胞生长.
结论:
- 在软矩阵上失败的粘附增强驱动了YAP介导的,依赖刚性的亡.
- 细胞命运的决定不仅取决于ECM的刚性,还取决于细胞力量和矩阵刚性的相互作用.
- 在细胞命运中,YAP扮演着双重的角色,在硬基质上调节增殖,在软基质上调节亡.
关键词:
CP: 细胞生物学 细胞生物学美国Src Src哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈这种药物是actomyosin.定位置-独立性的独立性.灭症 (apoptosis) 是一种死亡的过程.c-Ablbl 在线播放机械感知机械感知机器pYAP-Y357 这是一个很好的方法.刚性传感器 刚性传感器更多相关视频
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