ArticleJournal of the American Society of Nephrology : JASN2011
PKB/SGK-resistant GSK3 enhances phosphaturia and calciuria.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Contributions of SGK3 to transporter-related diseases.Frontiers in cell and developmental biology · 2022Review
- Insulin suppresses the production of fibroblast growth factor 23 (FGF23).Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Lack of serum- and glucocorticoid-inducible kinase 3 leads to podocyte dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- PI3K-resistant GSK3 controls adiponectin formation and protects from metabolic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Enhanced FGF23 production in mice expressing PI3K-insensitive GSK3 is normalized by β-blocker treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Checkpoint kinase Chk2 controls renal Cyp27b1 expression, calcitriol formation, and calcium-phosphate metabolism.Pflugers Archiv : European journal of physiology · 2015Article
- Upregulation of the Na⁺-coupled phosphate cotransporters NaPi-IIa and NaPi-IIb by B-RAF.The Journal of membrane biology · 2014Article
- The SLC34 family of sodium-dependent phosphate transporters.Pflugers Archiv : European journal of physiology · 2014Review
- Dynamic change of SGK expression and its role in neuron apoptosis after traumatic brain injury.International journal of clinical and experimental pathology · 2013Article
- Functional interaction between CFTR and the sodium-phosphate co-transport type 2a in Xenopus laevis oocytes.PloS one · 2012Article
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin and IGF1-dependent signaling activates protein kinase B and serum and glucocorticoid inducible kinase (PKB/SGK), which together phosphorylate and inactivate glycogen synthase kinase GSK3. Because insulin and IGF1 increase renal tubular calcium and phosphorus reabsorption, we examined GSK3 regulation of phosphate transporter activity and determined whether PKB/SGK inactivates GSK3 to enhance renal phosphate and calcium transport. Overexpression of GSK3 and the phosphate transporter NaPi-IIa in Xenopus oocytes decreased electrogenic phosphate transport compared with NaPi-IIa-expressing oocytes. PKB/SGK serine phosphorylation sites in GSK3 were mutated to alanine to create gsk3(KI) mice resistant to PKB/SGK inactivation. Compared with wildtype animals, gsk3(KI) animals exhibited greater urinary phosphate and calcium clearances with higher excretion rates and lower plasma concentrations. Isolated brush border membranes from gsk3(KI) mice showed less sodium-dependent phosphate transport and Na-phosphate co-transporter expression. Parathyroid hormone, 1,25-OH vitamin D levels, and bone mineral density were decreased in gsk3(KI) mice, suggesting a global dysregulation of bone mineral metabolism. Taken together, PKB/SGK phosphorylation of GSK3 increases phosphate transporter activity and reduces renal calcium and phosphate loss.
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