在InsP3受体和存储运行的Htrp3通道之间的功能相互作用
K Kiselyov1, X Xu, G Mozhayeva
1Department of Physiology, University of Texas Southwestern Medical Center at Dallas, 75235, USA.
Nature
|December 16, 1998
概括
储存运行的通道 (SOC) 通过消耗 (Ca2+) 储存而被激活. 这项研究表明,InsP3受体与Htrp3 SOC直接相互作用,调节Ca2+流入并支持细胞信号中的合假说.
科学领域:
- 细胞生物学 细胞生物学
- 分子信号传输的方法
- 离子通道生理学 离子通道生理学
背景情况:
- 离子 (Ca2+) 是重要的细胞内信使,在刺激时从储存中释放出来.
- 储存耗尽触发了通过储存运行的道 (SOC) 和Ca2+释放激活电流 (I ((crac)) 的Ca2+流入.
- 将Ca2+储量耗尽与SOC/I(crac) 激活联系在一起的机制仍在争论中,模型提出信使分子或直接受体合.
研究的目的:
- 为了研究存储运行的通道Htrp3和伊诺西1,4,5-三酸盐 (InsP3) 受体之间的功能相互作用.
- 为了确定InsP3受体是否直接调节SOC和I(crac) 活动,以应对Ca2+储量耗尽.
- 提供支持信号的合假设的证据.
主要方法:
- 哺乳动物Htrp3通道在HEK293细胞中的稳定表达.
- 在完整和切割的膜贴片中,SOC和I ((crac) 的电生理记录.
- 用InsP3进行刺激,并在Ca2+储量耗尽和受体洗后评估通道活性.
主要成果:
- Htrp3通道与InsP3受体具有紧密的功能相互作用.
- 在完整的细胞中 Ca2+ 调动和在切除的补丁中直接应用 InsP3 时观察到 Htrp3 通道激活.
- 在冲洗时丢失的InsP3诱导的Htrp3激活,通过添加与InsP3结合的InsP3受体恢复.
结论:
- 这些发现为信号中的合假设提供了有力的证据.
- 通过InsP3激活InsP3受体,直接与存储运行的通道 (SOC) 相互作用并调节它们.
- 这种直接相互作用机制对于在细胞内储存物耗尽后控制Ca2+流入至关重要.
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