In this issue of Cell Metabolism, Shibata et al. (2013) show that in renal intercalated cells mineralocorticoid receptors phosphorylated on serine 843 are rendered active by angiotensin-induced dephosphorylation. This finding represents a novel mechanism for regulating nuclear receptor activity, and explains the balance between Na-Cl reabsorption in response to volume depletion and K(+) excretion in response to potassium loading.
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