钙通道 Cav1.3 型 L 型钙通道门控调制的影响。
Impact of gating modulation in CaV1.3 L-type calcium channels.
机构信息
Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, Innsbruck, Austria.
出版信息
Channels (Austin). 2010 Nov-Dec;4(6):523-5. doi: 10.4161/chan.4.6.12872. Epub 2010 Nov 1.
Abstract
CaV1.3 L-type channels control inner hair cell (IHC) sensory and sinoatrial node (SAN) function, and excitability in central neurons by means of their low-voltage activation and inactivation properties. In SAN cells CaV1.3 inward calcium current (ICa) inactivates rapidly whereas in IHCs inactivation is slow. A candidate suggested in slowing CaV1.3 channel inactivation is the presynaptically located ribbon-synapse protein RIM that is expressed in immature IHCs in presynaptic compartments also expressing CaV1.3 channels. CaV1.3 channel gating is also modulated by an intramolecular C-terminal mechanism. This mechanism was elicited during analysis of human C-terminal splice variants that differ in the length of their C-terminus and that modulates the channel's negative activation range and slows calcium-dependent inactivation.
摘要
钙通道 Cav1.3 L 型通道通过其低压激活和失活特性来控制内耳毛细胞 (IHC) 的感觉和窦房结 (SAN) 功能以及中枢神经元的兴奋性。在 SAN 细胞中，Cav1.3 内向钙电流 (ICa) 快速失活，而在 IHCs 中失活较慢。一种被认为是减慢 Cav1.3 通道失活的候选物是位于突触前的带状突触蛋白 RIM，它在表达 Cav1.3 通道的突触前隔室中表达不成熟的 IHCs。Cav1.3 通道门控也受到分子内 C 末端机制的调节。在分析人类 C 末端剪接变体时发现了这种机制，这些变体在 C 末端的长度上有所不同，调节通道的负激活范围并减缓钙依赖性失活。
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