Disease relevance of Slc20a1

• Nicotinamide prevents the development of hyperphosphataemia by suppressing intestinal sodium-dependent phosphate transporter in rats with adenine-induced renal failure [1].

High impact information on Slc20a1

• Deletion mapping of nucleotide sequences mediating this inhibition led to the identification of a region that has previously been characterized as binding the pituitary-specific transcription factor Pit-1/GHF-1 [2].
• A full-length cDNA derived from a cDNA library of newborn rat lung probed with HG80 was the rat counterpart of sodium-dependent phosphate transporter type IIb and was designated rNaPi IIb [3].
• Recently, we demonstrated that STC1 stimulates, in an autocrine/paracrine fashion, bone mineralization by increasing phosphate uptake in osteoblasts apparently via the functional activity of the sodium-dependent phosphate transporter, Pit1 [4].
• Expression of rat PiT-1 in Xenopus oocytes revealed that it possesses Na+-dependent Pi cotransport activity [5].
• Molecular cloning and hormonal regulation of PiT-1, a sodium-dependent phosphate cotransporter from rat parathyroid glands [5].

Chemical compound and disease context of Slc20a1

• We evaluated the expression of the sodium-dependent phosphate transporter, NaPi-2, and the response to phosphonoformic acid (PFA) in rats with 5/6 nephrectomy-induced renal failure [6].

Anatomical context of Slc20a1

• PiT-1 messenger RNA (mRNA) is widely distributed in rat tissues and is most abundant in brain, bone, and small intestine [5].
• Phosphate uptake and PiT-1 protein expression in rat skeletal muscle [7].
• In contrast, PiT-1 and PiT-2 were detected at the basolateral membrane of hepatocytes [8].
• Regulation of phosphate (Pi) transport and NaPi-III transporter (Pit-1) mRNA in rat osteoblasts [9].
• Expression of this cDNA clone in the COS cell line has shown it to specifically encode a sodium-dependent phosphate transporter from bovine renal epithelial cells [10].

Associations of Slc20a1 with chemical compounds

• We tested the effects of extracellular Pi, Ca(2+) and IGF-I on Na(d)Pi transport and Pit-1 or Pit-2 mRNA expression in rat osteoblastic (PyMS) cells [9].
• These studies indicate that the combinatorial effects of FGF and FSK act through PKA, tyrosine kinase and MAP-kinase-dependent pathways, which target the inverted CCAAT, CRE, FRE and Pit-1 elements in the BSP gene to synergistically increase BSP expression [11].
• Some candidate genes for idiopathic hypercalciuria are suggested by the known physiology, including those encoding the vitamin D receptor, the 1 alpha-hydroxylase of vitamin D, the calcium-sensing receptor, the renal sodium-dependent phosphate transporter, and chloride channels, but others remain to be identified [12].
• A kinetic study revealed that the incubation with glutathione resulted in an increase of Km in the sodium-dependent phosphate transporter from 85 +/- 7.9 to 159 +/- 18 microM (n = 5, p less than 0.05) [13].
• Among molecules expressed in osteoblasts and known to be related to P(i) handling, stanniocalcin 1 was identified as an early response gene after foscarnet treatment; it was also regulated by extracellular P(i), and itself increased Pit1 accumulation in both osteoblast cultures and in vivo [14].

Regulatory relationships of Slc20a1

• IGF-I also stimulated Na(d)Pi transport and Pit-1 mRNA in primary rat calvarial osteoblasts [9].

Other interactions of Slc20a1

• Sodium-phosphate cotransporter (PiT-1) protein expression in soleus and red gastrocnemius were similar to each other and seven- to eightfold greater than PiT-1 expression in white gastrocnemius [7].
• In osteoblasts only the type III Na(+)-dependent phosphate (NaPi) transporter isoforms Pit-1 and Pit-2 have been identified [9].
• The urinary excretion of cAMP and PTH/PTH-related peptide (PTHrP) receptor and type II sodium-dependent phosphate transporter (NaPi-2) mRNA in the kidney were both decreased in rats fed the high P diets containing 1.2% or greater P [15].

Analytical, diagnostic and therapeutic context of Slc20a1

• Phosphate transporter protein expression was confirmed by Western blotting in basolateral and canalicular LPM and by immunofluorescence in intact liver [8].
• Using northern blot analysis, the PDGF-BB-enhanced Pi transporter (PiT) in A-10 cells was identified as Pit-1 (Glvr-1), a member of the type III Na-dependent PiT [16].
• Cloning, sequence analysis and expression of the cDNA encoding a sodium-dependent phosphate transporter from the bovine renal epithelial cell line NBL-1 [10].

References