Molecular Control of Growth-Related Sodium-Phosphate Co-transporter (SLC34A3)
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The type IIa sodium-dependent inorganic phosphate transporter (NaPi-IIa) has a central regulatory role in inorganic phosphate (Pi) homeostasis. Many studies have reported on the functions and regulatory mechanisms of NaPi-IIa. NaPi-IIc, however, was initially identified as a NaPi transporter required for growth in rodents. The gene encoding NaPi-IIc is causative for hereditary hypophosphatemic rickets with hypercalciuria and considered to be a critical NaPi transporter in the human kidney. However, the physiological roles and regulatory mechanisms of NaPi-IIc are not sufficiently elucidated. Recent studies show that NaPi-IIc is tightly regulated by a variety of agonists and physiological conditions via partially defined molecular mechanisms, including transcriptional and posttranscriptional regulation, protein phosphorylation, trafficking (endocytosis, exocytosis, and recycling), and the association of NaPi-IIc with interacting protein complexes. These data provide further information about understanding of human renal Pi handling. Here, we review recent findings regarding the molecular control of NaPi-IIc transporters.
KeywordsPhosphate Proximal tubules Brush border membrane Transporters Trafficking Human Rodents
This study was funded in part by the Ministry of Education, Culture, Sports, Science, and Technology of Japan (No. 23689045 to H. Segawa, No. 26293204 to K. Miyamoto), and the Salt Science Research Foundation (No. 1322 to K. Miyamoto).
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Conflict of Interest
Hiroko Segawa, Ichiro Kaneko, Yuji Shiozaki, Mikiko Ito, Sawako Tatsumi, and Ken-Ichi Miyamoto each declare no potential conflicts of interest.
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This article contains no studies with human and animal subjects performed by any of the authors.
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