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排序方式: 共有794条查询结果,搜索用时 31 毫秒
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Andreas W. Jehle Judith Forgo J. Biber Eleanor Lederer Reto Krapf Heini Murer 《Pflügers Archiv : European journal of physiology》1998,437(1):149-154
Insulin-like growth factor (IGF)-I and vanadate increase Na-dependent phosphate (Na/Pi) cotransport in opossum kidney (OK) cells. To gain more information about the mechanisms by which IGF-I and vanadate stimulate
Na/Pi-cotransport, we measured type II Na/Pi-cotransporter (NaPi-4) protein abundance by Western blot analysis and investigated the effects of protein synthesis and tyrosine
kinase inhibitors. The key findings in the present studies are as follows. First, incubation in IGF-I (10–8 M) and/or vanadate (10–3 M) for 3 h led to a non-additive 1.4-fold increase in Na/Pi-cotransport activity which was paralleled by a 1.5- to 2-fold increase in NaPi-4 protein. Second, actinomycin D did not abolish
the increase in Na/Pi-cotransport and cycloheximide did not prevent the IGF-I-induced increase in Na/Pi-cotransport and NaPi-4 protein. Third, among the protein kinase inhibitors tested, only staurosporine substantially reduced
the stimulation of Na/Pi-cotransport. In conclusion, the stimulatory effect of IGF-I on Na/Pi-cotransport is paralleled by an increased expression of NaPi-4 protein that is independent of protein synthesis and therefore
results from increased protein stability. The observation that IGF-I and/or vanadate lead to similar increases in Na/Pi-cotransport and NaPi-4 protein abundance provides further evidence that the stimulation of Na/Pi-cotransport by IGF-I and vanadate involves protein tyrosine phosphorylation of the same signalling molecules.
Received: 1 May 1998 / Received after revision: 25 August 1998 / Accepted: 1 September 1998 相似文献
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Laurent Beck Ralph A. Meyer Martha H. Meyer Jürg Biber Heini Murer Harriet S. Tenenhouse 《Pflügers Archiv : European journal of physiology》1996,431(6):936-941
The X-linked Gy mutation is closely linked, but not allelic, to Hyp and is characterized by rickets, hypophosphatemia, decreased renal tubular maximum for phosphate (Pi) reabsorption (TmP) and a specific reduction in renal brush-border membrane (BBM) Na+-Pi cotransport. Gy mice, like their normal littermates, respond to a low-Pi diet with an increase in BBM Na+-Pi cotransport, but fail to show an adaptive increase in Tmp. Using an antibody raised against the NH2 terminal peptide of the rat renal-specific Na+-Pi cotransporter (NaPi-2) and a NaPi-2 cDNA probe, we examined the effect of the Gy mutation and low-Pi diet (0.03% Pi) on NaPi-2 protein and mRNA abundance. The reduction in BBM Na+-Pi cotransport in Gy mice (51 ± 5% of normal, P < 0.05) was associated with a decrease in NaPi-2 protein (46 ± 12% of normal, P < 0.05) and mRNA abundance (76 ± 5%, P < 0.05). The low-Pi diet elicited a two- to three-fold increase in Na+-Pi cotransport in both normal and Gy mice that was accompanied by a large increase in NaPi-2 protein (10.2-fold in normal and 16.9-fold in Gy mice) and a modest increase in NaPi-2 mRNA (1.3-fold in both mouse strains, P < 0.05). The present data demonstrate that (1) the renal defect in BBM Pi transport in Gy mice can be ascribed to a deficit in NaPi-2 protein and mRNA abundance, (2) both normal and Gy mice respond to low Pi with an adaptive increase in NaPi-2 protein that exceeds the increase in Na+-Pi cotransport activity and NaPi-2 mRNA, (3) the adaptive increase in NaPi-2 protein and mRNA are not sufficient for the
overall increase in TmP following Pi restriction.
Received: 27 October 1995 / Received after revision: 4 December 1995 / Accepted: 6 December 1995 相似文献
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In recent years, two mammalian proximal tubular brush border membrane Na/Pi cotransporters (types I and II) have been structurally identified by expression cloning techniques. Oocyte expression studies
have shown that only the transport characteristics of the type II transporter correspond to the well-known properties of proximal
tubular brush border membrane of Pi transport. In studies on physiological regulation by hormonal and non-hormonal factors a direct involvement and determining
role of the type II transporter has been documented. Most interestingly, specific membrane retrieval/insertion phenomena participate
in acute (minutes/hours) adjustments of brush border membrane Na/Pi cotransport rates; for chronic (hours/days) alterations also specific resynthesis/degradation processes participate. In pathophysiological
alterations (e.g. in X-linked hypophosphataemia and in heavy metal-induced nephrotoxicity) the expression of the type II Na/Pi cotransporters is reduced and explains the observed phosphaturia. 相似文献
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The sodium phosphate cotransporter family SLC34 总被引:19,自引:3,他引:19
This review summarizes the characteristics of the solute carrier family SLC34 that is represented by the type ll Na/P(i)-cotransporters NaPi-lla (SLC34A1), NaPi-llb (SLC34A2) and NaPi-llc (SLC34A3). Other Na/P(i)-cotransporters are described within the SLC17 and SLC20 families. Type ll Na/P(i)-cotransporters are expressed in several tissues and play a major role in the homeostasis of inorganic phosphate. In kidney and small intestine, type ll Na/P(i)-cotransporters are located at the apical sites of epithelial cells and represent the rate limiting steps for transepithelial movement of phosphate. Physiological and pathophysiological regulation of renal and small intestinal epithelial transport of phosphate occurs through alterations in the abundance of type ll Na/P(i)-cotransporters. 相似文献
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