Schneider Eve R, Anderson Evan O, Gracheva Elena O, Bagriantsev Sviatoslav N
Department of Cellular & Molecular Physiology, Yale School of Medicine, New Haven, CT, USA.
Department of Cellular & Molecular Physiology, Yale School of Medicine, New Haven, CT, USA; Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale School of Medicine, New Haven, CT, USA.
Curr Top Membr. 2014;74:113-33. doi: 10.1016/B978-0-12-800181-3.00005-1.
At normal body temperature, the two-pore potassium channels TREK-1 (K2P2.1/KCNK2), TREK-2 (K2P10.1/KCNK10), and TRAAK (K2P4.1/KCNK2) regulate cellular excitability by providing voltage-independent leak of potassium. Heat dramatically potentiates K2P channel activity and further affects excitation. This review focuses on the current understanding of the physiological role of heat-activated K2P current, and discusses the molecular mechanism of temperature gating in TREK-1, TREK-2, and TRAAK.
在正常体温下,双孔钾通道TREK-1(K2P2.1/KCNK2)、TREK-2(K2P10.1/KCNK10)和TRAAK(K2P4.1/KCNK2)通过提供非电压依赖性钾离子泄漏来调节细胞兴奋性。热显著增强K2P通道活性并进一步影响细胞兴奋性。本综述聚焦于目前对热激活K2P电流生理作用的理解,并讨论TREK-1、TREK-2和TRAAK中温度门控的分子机制。