增长因子触发的脱化控制了葡萄糖脂素-莱克驱动的内细胞分裂
Ewan MacDonald1,2,3, Alison Forrester1,4,5, Cesar A Valades-Cruz1,6,7,8
1Cellular and Chemical Biology Unit, Institut Curie, Université PSL, U1143 INSERM, UMR3666 CNRS, Paris, France.
Nature cell biology
|February 21, 2025
概括
皮表皮生长因子通过触发快速的,依赖pH的糖蛋白的内细胞分裂,动态调节细胞粘附和迁移. 这个过程涉及神经aminidases和 galectins,为侵入性迁移重置细胞表面糖化.
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:
- 甘油脂-莱克相互作用调解了像β1整合素这样的货物的克拉特林独立内细胞分裂.
- 这种内细胞过程的动态调节在很大程度上仍未被探索.
研究的目的:
- 为了研究加勒激素驱动的内细胞分裂的动态调节.
- 阐明表皮生长因子 (EGF) 在触发这一过程中的作用.
- 了解控制细胞粘附,迁移和骨再吸收的分子机制.
主要方法:
- 研究了细胞表面糖蛋白的EGF触发的内细胞结核.
- 在这个过程中利用了Na+/H+抗载体 (NHE1) 和神经氨基酶 (Neu1, Neu3).
- 分析了pH触发的酸去除和随后的逆行运输到高尔基.
- 研究了神经氨基酶和加勒-3在骨再吸收中的作用.
主要成果:
- 在几分钟内,EGF迅速触发了像整体蛋白一样的葡萄糖蛋白的加勒素驱动的内细胞分裂.
- 该过程需要通过NHE1,Neu1和Neu3依赖于pH的去除酸,使其能够结合加勒素.
- 脱化葡萄糖蛋白在戈尔吉经历了糖重塑,调节了依赖EGF的侵入性迁移.
- 神经氨基酶和加勒-3都与依赖酸化的骨再吸收有关.
结论:
- 细胞表面糖化是一种动态的,可逆的修饰,可以控制适应性贩运途径.
- 这种机制调节了基本的细胞过程,包括粘附,迁移和骨质再吸收.
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