Clinical, biochemical, and pathophysiological analysis of SLC34A1 mutations-Reference-Cited by-同舟云学术

Clinical, biochemical, and pathophysiological analysis of SLC34A1 mutations

Published:2018-06 Issue:12 Volume:6 Page:e13715
ISSN:2051-817X
Container-title:Physiological Reports
language:en
Short-container-title:Physiol Rep

Author:

Fearn Amy¹,Allison Benjamin¹,Rice Sarah J.²,Edwards Noel²,Halbritter Jan³,Bourgeois Soline⁴,Pastor-Arroyo Eva M.⁴,Hildebrandt Friedhelm⁵,Tasic Velibor⁶,Wagner Carsten A.⁴,Hernando Nati⁴,Sayer John A.²⁷^ORCID,Werner Andreas¹

Affiliation:

1. Institute for Cell and Molecular Biosciences; Medical School; Newcastle University; Newcastle United Kingdom

2. Institute of Genetic Medicine; Newcastle University; Newcastle United Kingdom

3. Division of Nephrology; Department of Internal Medicine; University Clinic Leipzig; Leipzig Germany

4. Institute of Physiology; University of Zurich; Zurich Switzerland

5. Department of Medicine; Boston Children's Hospital; Harvard Medical School; Boston Massachusetts

6. Medical Faculty Skopje; University Children's Hospital; Skopje Macedonia

7. Renal Services; Newcastle Upon Tyne NHS Foundation Trust; Newcastle United Kingdom

Funder

Northern Counties Kidney Research Fund

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung

Publisher

Wiley

Subject

Physiology (medical),Physiology

Link

http://onlinelibrary.wiley.com/wol1/doi/10.14814/phy2.13715/fullpdf

Reference16 articles.

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3. Structural fold and binding sites of the human Na(+)-phosphate cotransporter NaPi-II;Fenollar-Ferrer;Biophys. J .,2014

4. Phosphate transporters in renal, gastrointestinal, and other tissues;Forster;Adv. Chronic. Kidney Dis.,2011

5. Fourteen monogenic genes account for 15% of nephrolithiasis/nephrocalcinosis;Halbritter;J. Am. Soc. Nephrol.,2015

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