TABLE 3.

SGK3 and sodium, chloride transport.

Cell type	Target	Result	Related disease
Xenopus oocytes	ENaC (epithelial sodium channel )	SGK3 could up-regulate the activity of ENaC. The epithelial sodium channel (ENaC) is mainly expressed in the kidney, lungs, salivary glands and skin, maintaining water and salt homeostasis, which can affect the reabsorption of sodium in the kidney, and regulating epithelial surface liquid volume in the respiratory
Brush-border membrane of the intestinal epithelium and the endosomal compartment	NHE3 (Na+/H+ exchanger 3)	SGK3 takes part in the Na+ reabsorption and H+ secretion of epithelial cells through NHE3 and play a role in the sodium transport and acid-base balance
Xenopus oocytes	Nav1.5, (SCN5A)	Co-expression of SGK3 and SCN5A could enhance the activity of SCN5A	Arrhythmia diseases
Xenopus oocytes	ClC-Ka and Nedd4-2	SGK3 up-regulated the ClC-Ka/barttin-induced currents, while Nedd4-2 down-regulated ClC-Ka/barttin activity, an effect reversed by SGK3	Loss of function of ClC-Ka/barttin channels results in idiopathic deafness and Bartter syndrome
Xenopus oocytes	ClC-2 and Nedd4-2	1. SGK3 could increase the activity and the number of ClC-2. SGK3 did not directly phosphorylate ClC-2 but regulated the activity and quantity of ClC-2 through the phosphorylation of Nedd4-2
		2. ClC-2 is widely distributed in the brain, heart, and gastrointestinal tract, involving in the regulation of neuronal excitability, chloride secretion and cell volume