Slc26a5 changes conformation in response to depolarization

The membrane protein Slc26a5 (prestin) contracts in the plane of the membrane in response to depolarization of the cell caused by opening of the mechanoelectrical transduction (MET) channel (Oliver et al. 2001, Gorbunov et al. 2014). Likewise, Slc26a5 expands in the plane of the membrane in response to hyperpolarization caused by MET channel closing. A current model for the reaction posits that association of anions (chloride or bicarbonate) with a binding pocket midway along the permeation pathway within Slc26a5 causes a change in the area occupied by SLC26A5 in the membrane (Oliver et al. 2001, Gorbunov et al. 2014). An influx of cations through the MET channel causes dissociation of anions from Slc26a5, reversing the conformational change (Oliver et al. 2001, Gorbunov et al. 2014). The contraction-elongation cycle of OHCs, due to conformational changes of prestin, provides feedback-amplification of the motions (principally the reticular lamina) of the organ of Corti.

细胞膜蛋白Slc26a5（预应力蛋白）在机械电转化（MET）通道开启引起的细胞去极化作用下，于细胞膜平面发生收缩（Oliver等，2001年，Gorbunov等，2014年）。同样地，当MET通道关闭导致超极化时，Slc26a5在细胞膜平面发生扩张。关于该反应的当前模型认为，阴离子（如氯离子或碳酸氢根离子）与Slc26a5渗透途径中部的结合口袋结合，导致SLC26A5在膜中占据的面积发生改变（Oliver等，2001年，Gorbunov等，2014年）。通过MET通道的阳离子流入导致阴离子从Slc26a5解离，从而逆转构象变化（Oliver等，2001年，Gorbunov等，2014年）。由于预应力蛋白的构象变化，外毛细胞（OHCs）的收缩-伸长周期为柯蒂器官的运动（主要指网状层）提供了反馈放大效应。