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. 2022 Dec 1;10:1007924. doi: 10.3389/fcell.2022.1007924

TABLE 4.

SGK3 and glucose, amino acid, and other substance transport.

Cell type Target Result Related disease
Xenopus oocytes and jejunum epithelial cells SGLT1 In vitro, SGK3 could increase the SGLT1 activity by phosphorylating Nedd4-2 and accelerate glucose absorption. In vivo, compared with SGK3 wild-type mice, the SGLT1 function and intestinal glucose transport of SGK3 knockout mice were impaired Diabetes and obesity
Xenopus oocytes SLC6A19 and Nedd4-2 SGK3 stimulated SLC6A19 activity and expression by influencing the ubiquitin ligase Nedd4-2 independently of 100Ser without modifying carrier substrate affinities
Xenopus oocytes ASCT2 SGK3 could up-regulate the expression and activity of ASCT2, thereby regulating the absorption of cellular nutrients
Xenopus oocytes and murine hippocampal neurones GluR1 SGK3 can up-regulate the GluR1 expression and activity in neuronal synapses and promote the transport of glutamate
Xenopus oocytes GluR6 SGK3 could also up-regulate the activity of GluR6, maintaining neuronal excitability and memory consolidation
Xenopus oocytes EAAT1, EAAT2, EAAT4, and EAAT5 SGK3 can stimulate the expression of excitatory amino acid transporters (EAAT1, EAAT2, EAAT4, and EAAT5) and contribute to glutamate uptake Loss of EAAT function and accumulation of glutamate is closely related to intractable temporal lobe epilepsy (TLE), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), glaucoma, and diabetic retinopathy
Xenopus oocytes SN1 (SLC38A3/SNAT3) and Nedd4-2 SGK3 can reverse the inhibition of SN1 by Nedd4-2 through phosphorylation and inhibition of Nedd4-2 Mice deficient of SN1 can cause ataxia and disorders in amino acid homeostasis and glucose metabolism
Xenopus oocytes CreaT and SLC6A8 SGK3 was a potent positive regulator of CreaT, which might regulate the creatine uptake CreaT defect could lead to seizures, intellectual disability, and language disorders
Xenopus oocytes NaDC1 SGK3 could enhance the activity of NaDC1, promoting renal tubular reabsorption of citrate Promoting the occurrence of calcium urolithiasis