Dear Xiaobin,

The following paper describes a work on slc34a3.

Am J Physiol Renal Physiol. 2009 Aug; 297(2): F350–F361.

Published online 2009 Jun 3. doi:  10.1152/ajprenal.90765.2008

PMCID: PMC2724260

Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency

Sophia Y. Breusegem,1 Hideaki Takahashi,1 Hector Giral-Arnal,1 Xiaoxin Wang,1 Tao Jiang,1 Jill W. Verlander,3 Paul Wilson,1 Shinobu Miyazaki-Anzai,1 Eileen Sutherland,1 Yupanqui Caldas,1 Judith T. Blaine,1 Hiroko Segawa,4 Ken-ichi Miyamoto,4 Nicholas P. Barry,1,2 and Moshe Levi1,2

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This article has been cited by other articles in PMC.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724260/

Abstract

Dietary potassium (K) deficiency is accompanied by phosphaturia and decreased renal brush border membrane (BBM) vesicle sodium (Na)-dependent phosphate (Pi) transport activity. Our laboratory previously showed that K deficiency in rats leads to increased abundance in the proximal tubule BBM of the apical Na-Pi cotransporter NaPi-IIa, but that the activity, diffusion, and clustering of NaPi-IIa could be modulated by the altered lipid composition of the K-deficient BBM (Zajicek HK, Wang H, Puttaparthi K, Halaihel N, Markovich D, Shayman J, Beliveau R, Wilson P, Rogers T, Levi M. Kidney Int 60: 694–704, 2001; Inoue M, Digman MA, Cheng M, Breusegem SY, Halaihel N, Sorribas V, Mantulin WW, Gratton E, Barry NP, Levi M. J Biol Chem 279: 49160–49171, 2004). Here we investigated the role of the renal Na-Picotransporters NaPi-IIc and PiT-2 in K deficiency. Using Western blotting, immunofluorescence, and quantitative real-time PCR, we found that, in rats and in mice, K deficiency is associated with a dramatic decrease in the NaPi-IIc protein abundance in proximal tubular BBM and in NaPi-IIc mRNA. In addition, we documented the presence of a third Na-coupled Pi transporter in the renal BBM, PiT-2, whose abundance is also decreased by dietary K deficiency in rats and in mice. Finally, electron microscopy showed subcellular redistribution of NaPi-IIc in K deficiency: in control rats, NaPi-IIc immunolabel was primarily in BBM microvilli, whereas, in K-deficient rats, NaPi-IIc BBM label was reduced, and immunolabel was prevalent in cytoplasmic vesicles. In summary, our results demonstrate that decreases in BBM abundance of the phosphate transporter NaPi-IIc and also PiT-2 might contribute to the phosphaturia of dietary K deficiency, and that the three renal BBM phosphate transporters characterized so far can be differentially regulated by dietary perturbations.

Keywords: hypokalemia, phosphaturia, SLC34A1, SLC34A3, SLC20A2

Hoping this will be helpful,

Rafik

Thanks Rafik for the info. This is an elite group in the field. It appears that the Slc34a3 antibody they used were made by their lab. I hope I can find such antibody for my research too.

Best,

Xiaobin