Vennekens R, Nilius B
Laboratory of Physiology, Katholieke Universiteit Leuven, Campus Gasthuisberg O/N1, Herestraat 49-Bus 802, 3000 Leuven, Belgium.
Handb Exp Pharmacol. 2007(179):269-85. doi: 10.1007/978-3-540-34891-7_16.
In the current review we will summarise data from the recent literature describing molecular and functional properties of TRPM4. Together with TRPM5, these channels are up till now the only molecular candidates for a class of non-selective, Ca(2+)-impermeable cation channels which are activated by elevated Ca2+ levels in the cytosol. Apart from intracellular Ca2+, TRPM4 activation is also dependent on membrane potential. Additionally, channel activity is modulated by ATP, phosphatidylinositol bisphosphate (PiP2), protein kinase C (PKC) phosphorylation and heat. The molecular determinants for channel activation, permeation and modulation are increasingly being clarified, and will be discussed here in detail. The physiological role of Ca(2+)-activated non-selective cation channels is unclear, especially in the absence of gene-specific knock-out mice, but evidence indicates a role as a regulator of membrane potential, and thus the driving force for Ca2+ entry from the extracellular medium.
在本综述中,我们将总结近期文献中有关TRPM4分子和功能特性的数据。与TRPM5一起,到目前为止,这些通道是一类非选择性、Ca(2+)不可渗透阳离子通道的唯一分子候选者,这类通道由胞质溶胶中升高的Ca2+水平激活。除了细胞内Ca2+外,TRPM4的激活还依赖于膜电位。此外,通道活性受ATP、磷脂酰肌醇二磷酸(PiP2)、蛋白激酶C(PKC)磷酸化和热的调节。通道激活、通透和调节的分子决定因素越来越清晰,将在本文中详细讨论。Ca(2+)激活的非选择性阳离子通道的生理作用尚不清楚,尤其是在缺乏基因特异性敲除小鼠的情况下,但有证据表明其作为膜电位调节剂的作用,从而作为Ca2+从细胞外介质进入的驱动力。