Rapid vesicular translocation and insertion of TRP channels
Rapid vesicular translocation and insertion of TRP channels
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DOI：
10.1038/ncb1150
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发表时间：
2004-08-01
影响因子：
21.3
通讯作者：
Clapham, DE
中科院分区：
文献类型：
--
作者：
Bezzerides, VJ;Ramsey, IS;Clapham, DE
广泛表达的瞬时受体电位（TRP）离子通道家族对阳离子具有渗透性，大多数导致细胞内钙离子增加。然而，它们的调节和门控并没有得到很好的理解。在这里，我们报告说，生长因子刺激启动快速易位的瞬时受体电位离子通道，TRPC 5，从囊泡举行储备下质膜。这个过程，我们称之为“快速囊泡插入TRP”（RiVIT），大大增加了膜相关的TRPC 5通道和功能TRPC 5电流，导致这些Ca 2+渗透性非选择性通道的严格时空控制。表皮生长因子（EGF）诱导的功能性TRP通道的掺入需要磷脂酰肌醇3-激酶（PI（3）K）、Rho GTdR Rac 1和磷脂酰肌醇4-磷酸5-激酶（PIP（5）K α）。TRPC 5可用性的增加影响培养的海马神经元中的轴突延伸速率，并且可能是启动响应于刺激的Ca 2+内流和细胞形态学变化的一般机制。
The broadly expressed transient receptor potential (TRP) family of ion channels are permeant to cations, most resulting in increased intracellular calcium. However, their regulation and gating is not well understood. Here, we report that growth factor stimulation initiates the rapid translocation of the transient receptor potential ion channel, TRPC5, from vesicles held in reserve just under the plasma membrane. This process, which we term 'rapid vesicular insertion of TRP' ( RiVIT), dramatically increases membrane-associated TRPC5 channels and functional TRPC5 current, resulting in tight spatial-temporal control of these Ca2+-permeant nonselective channels. Epidermal growth factor (EGF)-induced incorporation of functional TRP channels requires phosphatidylinositide 3-kinase (PI(3)K), the Rho GTPase Rac1 and phosphatidylinositol 4-phosphate 5-kinase (PIP(5)Kalpha). The increase in TRPC5 availability affects neurite extension rates in cultured hippocampal neurons, and may be a general mechanism for initiating Ca2+ influx and cell morphological changes in response to stimuli.