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  • Title: Cellular/molecular control of renal Na/Pi-cotransport.
    Author: Murer H, Forster I, Hilfiker H, Pfister M, Kaissling B, Lötscher M, Biber J.
    Journal: Kidney Int Suppl; 1998 Apr; 65():S2-10. PubMed ID: 9551425.
    Abstract:
    A type II Na/Pi-cotransporter located in the brush border membrane is the rate limiting and physiologically regulated step in proximal tubular phosphate (Pi) reabsorption. In states of altered Pi-reabsorption [for example, in response to parathyroid hormone (PTH) and to altered dietary intake of Pi or as a consequence of genetic abnormalities], brush border expression of the type II Na/Pi-cotransporter is accordingly modified. PTH initiates a regulatory cascade leading to membrane retrieval, followed by lysosomal degradation of this transporter; recovery from inhibition requires its de novo synthesis. Pi-deprivation leads to an increased brush border expression of transporters that does not appear to require de novo synthesis in the short term. Pi-overload leads to membrane retrieval and degradation of transporters. Finally, in animals with genetically altered Pi-handling (Hyp; Gy) the brush border membrane expression of the type II Na/Pi-cotransporter is also reduced, suggesting that a genetically altered protein (such as PEX in Hyp) controls the expression of this transporter.
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