细胞粘附分子uvomorulin的新功能是诱导细胞表面极性
Cell
|July 27, 1990
概括
像uvomorulin这样的细胞粘附分子 (CAM) 可以诱导细胞表面的极性. 这项研究表明,CAMs将Na+,K(+) -ATPase重新分配到细胞接触点,在发育和运输上皮细胞中建立极性.
科学领域:
- 细胞生物学 细胞生物学
- 发展生物学 发展生物学
- 分子生物学分子生物学
背景情况:
- 在介质细胞和上皮细胞之间,Na+,K(+) -ATPase的分布不同.
- 限制Na+,K(+) -ATPase局部化对于上皮细胞的发育和功能至关重要.
- 驱动这种有限的分销的机制在很大程度上是未知的.
研究的目的:
- 研究细胞粘附分子 (CAMs) 在确定细胞表面极性中的作用.
- 确定CAM表达是否可以诱导Na+,K(+) -ATPase的偏振分布.
主要方法:
- 纤维细胞被上皮CAM uvomorulin感染.
- 在转染细胞中分析Na+,K(+) -ATPase局部化.
- 研究膜细胞骨重组和紧密结节的形成.
主要成果:
- 纤维细胞中的uvomorulin表达诱导了Na+,K(+) -ATPase重分配到细胞与细胞接触.
- 这种重新分配是独立于紧密的连接而发生的.
- CAM诱导的极性与膜细胞骨架重组相吻合.
结论:
- 细胞粘附分子直接诱导细胞表面的极性.
- CAMs在膜和细胞质蛋白质的极化局部化中发挥着关键作用,例如Na+,K(+) -ATPase.
- 这一发现对理解表皮细胞发育和细胞极性有意义.
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