Qin F
Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, NY, USA.
Handb Exp Pharmacol. 2007(179):509-25. doi: 10.1007/978-3-540-34891-7_30.
Phosphatidylinositol-4,5-bisphosphate (PIP2) has emerged as a versatile regulator of TRP ion channels. In many cases, the regulation involves interactions of channel proteins with the lipid itself independent of its hydrolysis products. The functions of the regulation mediated by such interactions are diverse. Some TRP channels absolutely require PIP2 for functioning, while others are inhibited. A change of gating is common to all, endowing the lipid a role for modulation of the sensitivity of the channels to their physiological stimuli. The activation of TRP channels may also influence cellular PIP2 levels via the influx of Ca2+ through these channels. Depletion of PIP2 in the plasma membrane occurs upon activation of TRPV1, TRPM8, and possibly TRPM4/5 in heterologous expression systems, whereas resynthesis of PIP2 requires Ca2+ entry through the TRP/TRPL channels in Drosophila photoreceptors. These developments concerning PIP2 regulation of TRP channels reinforce the significance of the PLC signaling cascade in TRP channel function, and provide further perspectives for understanding the physiological roles of these ubiquitous and often enigmatic channels.
磷脂酰肌醇-4,5-二磷酸（PIP2）已成为一种多功能的瞬时受体电位（TRP）离子通道调节剂。在许多情况下，这种调节涉及通道蛋白与脂质本身的相互作用，而与其水解产物无关。这种相互作用介导的调节功能多种多样。一些TRP通道的正常功能绝对需要PIP2，而另一些则受到抑制。通道门控的改变是普遍存在的，赋予了脂质调节通道对其生理刺激敏感性的作用。TRP通道的激活还可能通过这些通道内流Ca2+来影响细胞内PIP2水平。在异源表达系统中，TRPV1、TRPM8以及可能还有TRPM4/5激活后，质膜中的PIP2会耗尽，而在果蝇光感受器中，PIP2的重新合成需要通过TRP/TRPL通道进入Ca2+。这些有关PIP2对TRP通道调节的进展强化了磷脂酶C（PLC）信号级联在TRP通道功能中的重要性，并为理解这些普遍存在且常常神秘的通道的生理作用提供了更多视角。
