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  • 1
    Electronic Resource
    Electronic Resource
    Role of rBAT Gene Products in Cystinuria (1996)
    Oxford, UK : Blackwell Publishing Ltd
    International journal of urology 3 (1996), S. 0 
    Details
    ISSN: 1442-2042
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To investigate whether rBAT gene products function as a crystine transporter component or as a transport activator, we microinjected several C–terminal deletion mutants of rBAT cRNA into Xenopus oocytes, and measured transport activity for arginine, leucine and cystine in the presence and absence of sodium. Wild type rBAT significantly stimulated the uptake of all 3 amino acids 10–20 fold compared to control mutants. On the other hand, no mutant, except a Δ511–685 mutant, stimulated the uptake of these amino acids. However, the Δ511–685 mutant significantly increased the uptake of arginine. In the presence of sodium, the Δ511–685 mutant also increased the uptake of leucine. The Δ511–685 mutant did not stimulate crystine uptake in the presence and absence of sodium. Furthermore, inhibition of L–arginine uptake by L–homoserine was seen only in the presence of sodium. These results suggest that mutant rBAT stimulates the endogenous amino acid transport system y+ in oocytes. Finally, rBAT gene products, as the primary cause of cystinuria, may function as activators of the amino acid transport system in renal brush border membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1442-2042.1996.tb00354.x
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  • 2
    Electronic Resource
    Electronic Resource
    Molecular and cellular regulation of renal phosphate transporters in X-linked hypophosphatemia (1998)
    Springer
    Clinical and experimental nephrology 2 (1998), S. 178-182 
    Details
    ISSN: 1437-7799
    Keywords: kidney ; phosphate ; hypophosphatemia ; mutation ; vitamin D ; transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Recent investigations of X-linked hypophosphatemia support the concept that the kidney is intrinsically normal in this disorder, and that the characteristic phosphaturia is caused by a humoral factor. The mechanisms involved in the pathophysiology of X-linked hypophosphatemia, Hyp, and oncogenic hypophosphatemic osteomalacia are complex and are the results of mutations in a putative zinc metalloprotease. Inactivation inPHEX gene function initiates a series of events that result in severe perturbations in renal Pi transport and metabolism of vitamin D. There are a number of possible working models that could explain the experimental observations. However, our studies clearly show that a humoral factor (phosphatonin) inhibits the transcription of the type II Na+/Pi cotransporter gene (Fig. 4). Phosphatonin may be a key modulator of phosphate homeostasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02480555
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of dietary phosphate on Na+-dependent phosphate cotransporters function and expression in the rat kidney (1998)
    Springer
    Clinical and experimental nephrology 2 (1998), S. 109-116 
    Details
    ISSN: 1437-7799
    Keywords: Na+-phosphate cotransporter ; dietary phosphate ; kidney ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background Three types (typeI, II, andIII) of sodium-dependent phosphate cotransporters have recently been isolated and shown to be expressed in the mammalian kidney. Understanding of the functional roles and regulation of each transporter is still fragmented, however. Methods We analyzed the functional roles of each transporter by using antisense oligonucleotides in theXenopus oocytes expression system, and by localization in the proximal tubules of rat kidney using immunohistochemistry. Results Phosphate uptake in brush border membranes was increased by about 2 times in rats fed a low-phosphate, as compared with a high-phosphate, diet. Expression of typeI, II, andIII transporter mRNAs was observed in renal poly(A)+RNA, isolated from the rats fed a low-phosphate diet. Phosphate uptake increased about 2.5-fold inXenopus oocytes injected with the poly(A)+RNA, compared with those given RNA from rats fed a high-phosphate diet. Hybrid depletion of the typeII sodium-dependent phosphate transporter (NaPi-2), but not of the typeI (rNaPi-1) or typeIII transporters (PiT-1 and PiT-2), significantly decreased phosphate transport activity in oocytes injected with the poly(A)+RNA from each experimental group rat kidney. In rats fed the lowphosphate diet, NaPi-2 immunoreactivity increased markedly in the brush border membranes of renal proximal tubular cells, whereas rNaPi-1 protein was not changed. Conclusion This study suggests that the typeII transporter functions mainly as a sodium-dependent phosphate cotransporter, and is regulated by dietary phosphate in the rat kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02479931
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  • 4
    Electronic Resource
    Electronic Resource
    Dietary regulation of renal phosphate transporters in hypophosphatemic mice (1998)
    Springer
    Journal of bone and mineral metabolism 16 (1998), S. 234-240 
    Details
    ISSN: 1435-5604
    Keywords: Key words: hypophosphatemia ; Na-dependent phosphate cotransporter ; kidney ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: X-linked hypophosphatemic rickets (XLH) is known to impair renal adaptive response to Pi restriction. We investigated the effects of dietary Pi on the synthesis of renal sodium-dependent inorganic phosphate (Na/Pi) cotransporters (Npt1 and NaPi-7) in X-linked hypophosphatemic mice (Hyp). The NaPi-7 mRNA level in Hyp mice was reduced to 50% of that of normal mice while the Npt1 mRNA level was unchanged. After feeding a low-Pi diet, the amounts of NaPi-7 protein and mRNA were markedly increased in both normal and Hyp mice. In contrast, after feeding a high-Pi diet, the levels of protein and mRNA were largely decreased in both mice. Immunohistochemical analysis indicated that NaPi-7 staining was largely enhanced in the apical membrane of renal proximal tubular cells in the normal and Hyp mice fed the low-Pi diet. In contrast, NaPi-7 staining was decreased in both groups of rats fed the high-Pi diet. Npt1 immunoreactivity was detected in the apical membrane of proximal convoluted and straight tubular cells in Hyp and normal mice, and was unchanged regardless of dietary Pi manipulation in both mice. Thus, dietary regulation for the synthesis of the two cotransporters is not impaired in Hyp mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007740050050
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