Deletion of KS-WNK1 promotes NCC activation by increasing WNK1/4 abundance

In this paper, we show that KS-WNK1 is a critical component of the distal convoluted tubule (DCT) K + switch pathway. Its deletion results in an inability of the DCT to sense changes in plasma potassium. Absence of KS-WNK1 leads to abnormally high levels of WNK4 and L-WNK1 in the DCT, resulting in increased Na-Cl phosphorylation and function. Our data are consistent with KS-WNK1 targeting WNK4 and L-WNK1 to degradation.