存储运行的Ca2+输入:证据表明一种分泌类合模型
R L Patterson1, D B van Rossum, D L Gill
1Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore 21201, USA.
Cell
|September 11, 1999
概括
这项研究揭示了内质网膜 (ER) 和血膜 (PM) 通过物理,可逆的机制进行通信. 动氨酸细胞骨重组会破坏这种 (Ca2+) 信号通路,但其正常功能可以恢复.
科学领域:
- 细胞生物学 细胞生物学
- 信号传递 信号传递
- 膜动力学 膜动力学
背景情况:
- 连接内细胞网膜 (ER) (Ca2+) 储存与血膜 (PM) Ca2+通道的精确机制仍然不完全理解.
- 储存运行进入 (SOCE) 是一个由ER Ca2+储存和PM通道之间的通信调节的关键过程.
研究的目的:
- 调查细胞骨,特别是动氨酸纤维在介导ER Ca2+储存和PM Ca2+通道之间的合中的作用.
- 阐明ER和PM之间信号传输通信的物理基础.
主要方法:
- 利用细胞骨修饰,包括丝破坏和重新分配,以探测ER-PM合.
- 观察了这些修改对Ca2+进入通道和因诺西1,4,5-三酸盐介导的储存释放的影响.
主要成果:
- 动氨酸细胞骨的分解没有影响ER-PM合.
- 将F-actin重新分配到细胞皮层中,取代了ER,破坏了合并阻止了Ca2+的进入,但没有影响因诺西1,4,5-三酸盐诱导的Ca2+释放.
- 逆转了行动蛋白皮质层的形成,恢复了ER-PM的接近和合.
结论:
- ER和PM之间的信号合是由一个物理,类似分泌的机制介导的,涉及密切的,可逆的相互作用.
- 动蛋白细胞骨在调节ER和PM的接近性和功能性合以进入方面发挥着至关重要的作用.
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