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Physiological Reviews, Vol. 80, No. 4, October 2000, pp. 1373-1409
Copyright ©2000 by the American Physiological Society
Institute of Physiology, University of Zürich, Zürich, Switzerland
Murer, Heini,
Nati Hernando,
Ian Forster, and
Jürg Biber.
Proximal Tubular Phosphate Reabsorption: Molecular
Mechanisms. Physiol. Rev. 80: 1373-1409, 2000.
Renal
proximal tubular reabsorption of Pi is a key element in
overall Pi homeostasis, and it involves a secondary active
Pi transport mechanism. Among the molecularly identified
sodium-phosphate (Na/Pi) cotransport systems a
brush-border membrane type IIa Na-Pi cotransporter is
the key player in proximal tubular Pi reabsorption. Physiological and pathophysiological alterations in renal
Pi reabsorption are related to altered brush-border
membrane expression/content of the type IIa Na-Pi
cotransporter. Complex membrane retrieval/insertion mechanisms are
involved in modulating transporter content in the brush-border
membrane. In a tissue culture model (OK cells) expressing intrinsically
the type IIa Na-Pi cotransporter, the cellular cascades involved in "physiological/pathophysiological" control of
Pi reabsorption have been explored. As this cell model
offers a "proximal tubular" environment, it is useful for
characterization (in heterologous expression studies) of the
cellular/molecular requirements for transport regulation. Finally, the
oocyte expression system has permitted a thorough characterization of
the transport characteristics and of structure/function relationships.
Thus the cloning of the type IIa Na-Pi cotransporter (in
1993) provided the tools to study renal brush-border membrane
Na-Pi cotransport function/regulation at the
cellular/molecular level as well as at the organ level and led to an
understanding of cellular mechanisms involved in control of proximal
tubular Pi handling and, thus, of overall Pi homeostasis.
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G. Lambert, I. C. Forster, G. Stange, K. Kohler, J. Biber, and H. Murer Cysteine Mutagenesis Reveals Novel Structure-Function Features within the Predicted Third Extracellular Loop of the Type Iia Na+/Pi Cotransporter J. Gen. Physiol., June 1, 2001; 117(6): 533 - 546. [Abstract] [Full Text] [PDF]
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G. J. Strewler FGF23, hypophosphatemia, and rickets: Has phosphatonin been found? PNAS, May 22, 2001; 98(11): 5945 - 5946. [Full Text] [PDF]
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L. D. Quarles Pathophysiology of X-Linked Hypophosphatemia, Tumor-Induced Osteomalacia, and Autosomal Dominant Hypophosphatemia: A PerPHEXing Problem J. Clin. Endocrinol. Metab., February 1, 2001; 86(2): 494 - 496. [Full Text]
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Z. Karim-Jimenez, N. Hernando, J. Biber, and H. Murer A dibasic motif involved in parathyroid hormone-induced down-regulation of the type IIa NaPi cotransporter PNAS, October 23, 2000; (2000) 220394197. [Abstract] [Full Text]
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S. M. Gisler, I. Stagljar, M. Traebert, D. Bacic, J. Biber, and H. Murer Interaction of the Type IIa Na/Pi Cotransporter with PDZ Proteins J. Biol. Chem., March 16, 2001; 276(12): 9206 - 9213. [Abstract] [Full Text] [PDF]
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Z. Karim-Jimenez, N. Hernando, J. Biber, and H. Murer A dibasic motif involved in parathyroid hormone-induced down-regulation of the type IIa NaPi cotransporter PNAS, November 7, 2000; 97(23): 12896 - 12901. [Abstract] [Full Text] [PDF]
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Y. Soumounou, C. Gauthier, and H. S. Tenenhouse Murine and human type I Na-phosphate cotransporter genes: structure and promoter activity Am J Physiol Renal Physiol, December 1, 2001; 281(6): F1082 - F1091. [Abstract] [Full Text] [PDF]
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W. Wang, T.-H. Kwon, C. Li, J. Frokiar, M. A. Knepper, and S. Nielsen Reduced expression of Na-K-2Cl cotransporter in medullary TAL in vitamin D-induced hypercalcemia in rats Am J Physiol Renal Physiol, January 1, 2002; 282(1): F34 - F44. [Abstract] [Full Text] [PDF]
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K. Kohler, I. C. Forster, G. Stange, J. Biber, and H. Murer Identification of functionally important sites in the first intracellular loop of the NaPi-IIa cotransporter Am J Physiol Renal Physiol, April 1, 2002; 282(4): F687 - F696. [Abstract] [Full Text] [PDF]
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