ArticleProceedings of the National Academy of Sciences of the United States of America2000
A dibasic motif involved in parathyroid hormone-induced down-regulation of the type IIa NaPi cotransporter.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- The molecular sociology of NHERF1 PDZ proteins controlling renal hormone-regulated phosphate transport.Bioscience reports · 2024Article
- The Effects of Acid on Calcium and Phosphate Metabolism.International journal of molecular sciences · 2024Review
- Physiopathology of Phosphate Disorders.Advances in kidney disease and health · 2023Review
- Does the composition of urinary extracellular vesicles reflect the abundance of renal NaPflugers Archiv : European journal of physiology · 2022Article
- NaPi-IIa interacting partners and their (un)known functional roles.Pflugers Archiv : European journal of physiology · 2019Review
- Physiological regulation of phosphate by vitamin D, parathyroid hormone (PTH) and phosphate (Pi).Pflugers Archiv : European journal of physiology · 2019Review
- Exome sequencing identifies a novel homozygous mutation in the phosphate transporter SLC34A1 in hypophosphatemia and nephrocalcinosis.The Journal of clinical endocrinology and metabolism · 2014Article
- Intestinal phosphate transport.Advances in chronic kidney disease · 2011Article
- Acute parathyroid hormone differentially regulates renal brush border membrane phosphate cotransporters.Pflugers Archiv : European journal of physiology · 2010Article
- Regulation of phosphate transport in proximal tubules.Pflugers Archiv : European journal of physiology · 2009Review
- Evidence for a signaling axis by which intestinal phosphate rapidly modulates renal phosphate reabsorption.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis.American journal of human genetics · 2006Article
- Secreted frizzled-related protein-4 reduces sodium-phosphate co-transporter abundance and activity in proximal tubule cells.Pflugers Archiv : European journal of physiology · 2006Article
- NaPi-IIa and interacting partners.The Journal of physiology · 2005Review
- Interaction of a farnesylated protein with renal type IIa Na/Pi co-transporter in response to parathyroid hormone and dietary phosphate.The Biochemical journal · 2004Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Type II NaPi cotransporters are expressed in the apical membrane of P(i)-(re)absorbing epithelia: the type IIa in renal proximal tubule and the type IIb in small intestine. Parathyroid hormone (PTH) leads to a retrieval from the apical membrane of the type IIa NaPi cotransporter. The type IIa cotransporter is also expressed in opossum kidney (OK) cells, and its expression is under the control of PTH. In the present study, we identified the molecular "domains" involved in the PTH-induced retrieval of the type IIa NaPi cotransporter. Wild-type mouse type IIa (mIIa) and type IIb (mIIb) as well as several mIIa-mIIb chimeras and site-directed mutants were fused to the enhanced green fluorescent protein and transfected into OK cells. We found that mIIa but not mIIb was internalized and degraded after incubation with 1-34 (or 3-34) PTH. Using chimeras, we found that the N and C termini were not required in this effect, whereas a "domain" located between residues 216 and 658 seemed to be necessary. This region contains two putative intracellular loops with highly conserved sequences between mIIa and mIIb; in the last intracellular loop, two charged amino acids of type IIa (K(503)R(504)) are replaced by uncharged residues in type IIb (N(520)I(521)). We generated two mutants in which these residues were interchanged: mIIaNI and mIIbKR. Similarly to mIIa, the mIIbKR mutant was endocytosed in response to 1-34 PTH; in contrast, mIIaNI behaved as mIIb and was not internalized. In conclusion, a dibasic amino acid motif (K(503)R(504)) located in the last intracellular loop of the type IIa NaPi cotransporter is essential for its PTH-induced retrieval.
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