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Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure.

Soleimani M, Barone S, Xu J, Shull GE, Siddiqui F, Zahedi K, Amlal H.

Proc Natl Acad Sci U S A. 2012 Aug 14;109(33):13368-73. doi: 10.1073/pnas.1202671109. Epub 2012 Jul 30.


A novel target for diuretic therapy.

Soleimani M.

Iran J Kidney Dis. 2012 Nov;6(6):419-25.


Pendrin as a novel target for diuretic therapy.

Amlal H, Soleimani M.

Cell Physiol Biochem. 2011;28(3):521-6. doi: 10.1159/000335117. Epub 2011 Nov 18. Review.


Double knockout of carbonic anhydrase II (CAII) and Na(+)-Cl(-) cotransporter (NCC) causes salt wasting and volume depletion.

Xu J, Barone S, Brooks MB, Soleimani M.

Cell Physiol Biochem. 2013;32(7):173-83. doi: 10.1159/000356637. Epub 2013 Dec 18.


The Role of Epithelial Sodium Channel ENaC and the Apical Cl-/HCO3- Exchanger Pendrin in Compensatory Salt Reabsorption in the Setting of Na-Cl Cotransporter (NCC) Inactivation.

Patel-Chamberlin M, Varasteh Kia M, Xu J, Barone S, Zahedi K, Soleimani M.

PLoS One. 2016 Mar 10;11(3):e0150918. doi: 10.1371/journal.pone.0150918. eCollection 2016.


The multiple roles of pendrin in the kidney.

Soleimani M.

Nephrol Dial Transplant. 2015 Aug;30(8):1257-66. doi: 10.1093/ndt/gfu307. Epub 2014 Oct 3. Review.


Expression and phosphorylation of the Na+-Cl- cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1.

Vallon V, Schroth J, Lang F, Kuhl D, Uchida S.

Am J Physiol Renal Physiol. 2009 Sep;297(3):F704-12. doi: 10.1152/ajprenal.00030.2009. Epub 2009 Jul 1.


Reduced ENaC protein abundance contributes to the lower blood pressure observed in pendrin-null mice.

Kim YH, Pech V, Spencer KB, Beierwaltes WH, Everett LA, Green ED, Shin W, Verlander JW, Sutliff RL, Wall SM.

Am J Physiol Renal Physiol. 2007 Oct;293(4):F1314-24. Epub 2007 Aug 8.


The role of pendrin in renal physiology.

Wall SM, Lazo-Fernandez Y.

Annu Rev Physiol. 2015;77:363-78. doi: 10.1146/annurev-physiol-021014-071854. Review.


Potentiation of the effect of thiazide derivatives by carbonic anhydrase inhibitors: molecular mechanisms and potential clinical implications.

Zahedi K, Barone S, Xu J, Soleimani M.

PLoS One. 2013 Nov 18;8(11):e79327. doi: 10.1371/journal.pone.0079327. eCollection 2013.


Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension.

Ronzaud C, Loffing-Cueni D, Hausel P, Debonneville A, Malsure SR, Fowler-Jaeger N, Boase NA, Perrier R, Maillard M, Yang B, Stokes JB, Koesters R, Kumar S, Hummler E, Loffing J, Staub O.

J Clin Invest. 2013 Feb;123(2):657-65. doi: 10.1172/JCI61110. Epub 2013 Jan 25.


Impaired phosphorylation of Na(+)-K(+)-2Cl(-) cotransporter by oxidative stress-responsive kinase-1 deficiency manifests hypotension and Bartter-like syndrome.

Lin SH, Yu IS, Jiang ST, Lin SW, Chu P, Chen A, Sytwu HK, Sohara E, Uchida S, Sasaki S, Yang SS.

Proc Natl Acad Sci U S A. 2011 Oct 18;108(42):17538-43. doi: 10.1073/pnas.1107452108. Epub 2011 Oct 4.


Generation and analysis of the thiazide-sensitive Na+ -Cl- cotransporter (Ncc/Slc12a3) Ser707X knockin mouse as a model of Gitelman syndrome.

Yang SS, Lo YF, Yu IS, Lin SW, Chang TH, Hsu YJ, Chao TK, Sytwu HK, Uchida S, Sasaki S, Lin SH.

Hum Mutat. 2010 Dec;31(12):1304-15. doi: 10.1002/humu.21364. Epub 2010 Oct 14.


Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl(-)/HCO3(-) exchanger activity and impairs bicarbonate secretion in kidney collecting duct.

Amlal H, Petrovic S, Xu J, Wang Z, Sun X, Barone S, Soleimani M.

Am J Physiol Cell Physiol. 2010 Jul;299(1):C33-41. doi: 10.1152/ajpcell.00033.2010. Epub 2010 Apr 7.


Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice.

Sorensen MV, Grossmann S, Roesinger M, Gresko N, Todkar AP, Barmettler G, Ziegler U, Odermatt A, Loffing-Cueni D, Loffing J.

Kidney Int. 2013 May;83(5):811-24. doi: 10.1038/ki.2013.14. Epub 2013 Feb 27.


Deletion of the Cl-/HCO3- exchanger pendrin downregulates calcium-absorbing proteins in the kidney and causes calcium wasting.

Barone S, Amlal H, Xu J, Soleimani M.

Nephrol Dial Transplant. 2012 Apr;27(4):1368-79. doi: 10.1093/ndt/gfr505. Epub 2011 Aug 26.


Phenotype resembling Gitelman's syndrome in mice lacking the apical Na+-Cl- cotransporter of the distal convoluted tubule.

Schultheis PJ, Lorenz JN, Meneton P, Nieman ML, Riddle TM, Flagella M, Duffy JJ, Doetschman T, Miller ML, Shull GE.

J Biol Chem. 1998 Oct 30;273(44):29150-5.


Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

Faresse N, Lagnaz D, Debonneville A, Ismailji A, Maillard M, Fejes-Toth G, Náray-Fejes-Tóth A, Staub O.

Am J Physiol Renal Physiol. 2012 Apr 15;302(8):F977-85. doi: 10.1152/ajprenal.00535.2011. Epub 2012 Feb 1.


Inactivation of the Na-Cl co-transporter (NCC) gene is associated with high BMD through both renal and bone mechanisms: analysis of patients with Gitelman syndrome and Ncc null mice.

Nicolet-Barousse L, Blanchard A, Roux C, Pietri L, Bloch-Faure M, Kolta S, Chappard C, Geoffroy V, Morieux C, Jeunemaitre X, Shull GE, Meneton P, Paillard M, Houillier P, De Vernejoul MC.

J Bone Miner Res. 2005 May;20(5):799-808. Epub 2004 Dec 27.


mPGES-1 deletion impairs aldosterone escape and enhances sodium appetite.

Jia Z, Aoyagi T, Kohan DE, Yang T.

Am J Physiol Renal Physiol. 2010 Jul;299(1):F155-66. doi: 10.1152/ajprenal.90702.2008. Epub 2010 Mar 24.

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