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首页> 外文期刊>Neuron >Alternative translation initiation in rat brain yields K2P2.1 potassium channels permeable to sodium.
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Alternative translation initiation in rat brain yields K2P2.1 potassium channels permeable to sodium.

机译:大鼠大脑中的其他翻译起始产生了钠可渗透的K2P2.1钾通道。

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摘要

K(2P) channels mediate potassium background currents essential to central nervous system function, controlling excitability by stabilizing membrane potential below firing threshold and expediting repolarization. Here, we show that alternative translation initiation (ATI) regulates function of K(2P)2.1 (TREK-1) via an unexpected strategy. Full-length K(2P)2.1 and an isoform lacking the first 56 residues of the intracellular N terminus (K(2P)2.1Delta1-56) are produced differentially in a regional and developmental manner in the rat central nervous system, the latter passing sodium under physiological conditions leading to membrane depolarization. Control of ion selectivity via ATI is proposed to be a natural, epigenetic mechanism for spatial and temporal regulation of neuronal excitability.
机译:K(2P)通道介导中枢神经系统功能必不可少的钾背景电流,通过将膜电位稳定在激发阈值以下并加速复极化来控制兴奋性。在这里,我们显示了替代翻译起始(ATI)通过意外策略调节K(2P)2.1(TREK-1)的功能。全长K(2P)2.1和缺乏胞内N端的前56个残基的同工型(K(2P)2.1Delta1-56)在大鼠中枢神经系统中以区域和发育方式产生差异,后者通过钠在生理条件下导致膜去极化。提出通过ATI控制离子选择性是一种自然的,表观遗传的神经元兴奋性时空调节机制。

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