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TRIC channels are essential for Ca~(2+) handling in intracellular stores

机译：TRIC通道对于细胞内存储中的Ca〜（2+）处理至关重要

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摘要

Cell signalling requires efficient Ca~(2+) mobilization from intracellular stores through Ca~(2+) release channels, as well as predicted counter-movement of ions across the sarcoplasmic/endoplasmic reticulum membrane to balance the transient negative potential generated by Ca~(2+) release. Ca~(2+) release channels were cloned more than 15 years ago, whereas the molecular identity of putative counter-ion channels remains unknown. Here we report two TRIC (trimeric intracellular cation) channel subtypes that are differentially expressed on intracellular stores in animal cell types. TRIC subtypes contain three proposed transmembrane segments, and form homo-trimers with a bullet-like structure. Electrophysi-ological measurements with purified TRIC preparations identify a monovalent cation-selective channel. In TRIC-knockout mice suffering embryonic cardiac failure, mutant cardiac myocytes show severe dysfunction in intracellular Ca~(2+) handling. The TRIC-deficient skeletal muscle sarcoplasmic reticulum shows reduced K~+ permeability, as well as altered Ca~(2+) 'spark' signalling and voltage-induced Ca~(2+) release. Therefore, TRIC channels are likely to act as counter-ion channels that function in synchronization with Ca~(2+) release from intracellular stores.
机译：细胞信号传递需要通过Ca〜（2+）释放通道从细胞内存储区有效地调动Ca〜（2+），以及预测离子穿过肌浆/内质网膜的反向运动，以平衡Ca〜产生的瞬时负电位。 （2+）版本。 Ca〜（2+）释放通道已被克隆超过15年，而推定的抗衡离子通道的分子身份仍然未知。在这里，我们报告两种TRIC（三聚体细胞内阳离子）通道亚型，它们在动物细胞类型的细胞内储存物中差异表达。 TRIC亚型包含三个建议的跨膜片段，并形成具有子弹状结构的均三聚体。纯化的TRIC制剂的电生理学测量可确定单价阳离子选择性通道。在遭受胚胎性心力衰竭的TRIC基因敲除小鼠中，突变型心肌细胞在细胞内Ca〜（2+）处理中表现出严重的功能障碍。缺乏TRIC的骨骼肌肌质网显示K〜+渗透性降低，以及Ca〜（2+）``火花''信号和电压诱导的Ca〜（2+）释放改变。因此，TRIC通道很可能充当反离子通道，与细胞内存储中的Ca〜（2+）释放同步发挥作用。

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