FAK和p130Cas调节硬度介导的早期转录和细胞代谢
Bat-Ider Tumenbayar1, Vincent M Tutino2,3,4, Joseph A Brazzo2
1Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USA.
bioRxiv : the preprint server for biology
|January 31, 2024
概括
细胞代谢是由细胞外基质 (ECM) 刚性调节的. 焦点粘附激酶 (FAK) 和p130Cas信号传递介导了ECM刚性如何影响早期基因表达和细胞代谢.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 机械生物学 机械生物学
背景情况:
- 细胞代谢受到细胞外基质 (ECM) 的机械性质的显著影响.
- 焦粘附激酶 (FAK) 和其结合伙伴p130Cas在调解早期转录和代谢对ECM刚性的反应中的作用尚不清楚.
- 已知FAK和p130Cas从基质传递生物机械信号到细胞,调节各种细胞功能.
研究的目的:
- 研究ECM硬度对细胞早期转录反应的影响.
- 确定焦点粘附激酶 (FAK) 和p130Cas在调解这些反应中的参与.
- 阐明FAK-p130Cas信号如何影响细胞代谢和生物合成在不同的基质刚度下.
主要方法:
- 小鼠胚胎纤维细胞被培养并接受了siRNA介导的FAK或p130Cas.的淘汰.
- 然后在不同硬度 (软硬) 的基板上培养细胞.
- 使用RNA测序和生物信息学分析分析了早期的转录反应.
主要成果:
- 暴露于刚性ECM显著改变了参与代谢和生物合成途径的基因表达.
- 击败FAK和p130Cas影响了这些ECM硬度依赖的转录变化.
- 鉴定出FAK-p130Cas信号传递是ECM硬度对基因表达的影响的关键调解者.
结论:
- FAK-p130Cas信号传递是ECM刚性如何影响细胞转录程序的关键调解器.
- 这些信号通路在响应机械线索时,启动细胞代谢和生物合成的变化.
- 了解这种机械传导途径可以了解细胞矩阵相互作用和代谢调节.
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