The kinase, ULK1, is highly expressed in ICs and mediates the phosphorylation of the IC MR at S843. Upon angiotensin II binding to the angiotensin type 1 receptor (AT1R), mTOR phosphorylates, and thus inactivates, ULK1. With this ULK1 inactivation, the MR is dephosphorylated at S843, which enhances aldosterone binding to the MR. The IC MR is therefore activated and thus translocates to the nucleus, which stimulates gene transcription.