Novel strategy to regulate renal channels and transporters

本研究的目的是阐明肾脏转运体和通道的新的调控机制，特别是水通道、氯离子通道和SLC12A转运体，并试图开发新的策略来治疗这些转运体和通道调节失调所引起的疾病。我们阐明了AQP11缺失导致肾囊肿形成的分子机制，确定了拯救内质网(ER)残留致病突变体Barttin的药物，并分离出了一些抑制WNK-OSR1/Spak-SLC12A信号转导的化合物。

The purpose of our study was to clarify novel regulatory mechanisms of renal transporters and channels, especially AQP water channels, CLC chloride channels, and SLC12A transporters, and to try to develop new strategy to treat diseases caused by the dysregulation of these transporters and channels. We clarified the molecular pathogenesis of renal cyst formation caused by the deletion of AQP11, identified the agents to rescue endoplasmic reticulum (ER)-retained disease-causing mutant Barttin, and isolated some chemical compounds that inhibited WNK-OSR1/SPAK-SLC12A signaling.