通过整合素介导的Cdc42激活控制了通过PKCzeta迁移天体细胞中的细胞极性
1MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, WC1E 6BT, London, United Kingdom.
Cell
|August 30, 2001
概括
细胞损伤触发了一个信号通路,该通路确定了哺乳动物细胞的极性. 集成因介导的信号激活Cdc42,招募Park6/PKCzeta复合体,这对于细胞重组和定向迁移至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 信号传输 信号传输
背景情况:
- 细胞极性对组织组织和组织功能至关重要.
- 了解细胞极性建立的分子机制是细胞生物学的一个关键领域.
研究的目的:
- 为了阐明控制哺乳动物细胞极性信号传导途径.
- 识别关键分子参与细胞损伤和随后的极化反应的参与者.
主要方法:
- 诱导细胞极性通过划伤初级大鼠天体细胞的交汇单层.
- 研究整合素,Cdc42,mPar6/PKCzeta复合体和dynein在极化过程中的作用.
- 显微镜和生物化学分析分析细胞重组和蛋白质招募.
主要成果:
- 划伤诱导了细胞两极分化,有机体重组到前沿.
- 集成蛋白与细胞外矩阵的相互作用激活了Cdc42,它招募并激活了mPar6/PKCzeta复合体.
- 局部PKCzeta活性,通过dynein调解,对于所有观察到的诱导极性方面至关重要.
结论:
- 已经确定了一种用于确定哺乳动物细胞极性的一种新信号传导途径.
- 该途径涉及整合素信号传导,Cdc42,mPar6/PKCzeta复合体,以及dynein.
- 这一途径对于细胞损伤后的定向细胞突起和迁移至关重要.
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