Deletion of claudin-10 rescues claudin-16-deficient mice from hypomagnesemia and hypercalciuria.

[1]  C. Bodemer,et al.  Multiplex epithelium dysfunction due to CLDN10 mutation: the HELIX syndrome , 2017, Genetics in Medicine.

[2]  E. Bongers,et al.  A Novel Hypokalemic-Alkalotic Salt-Losing Tubulopathy in Patients with CLDN10 Mutations. , 2017, Journal of the American Society of Nephrology : JASN.

[3]  S. Baig,et al.  Altered paracellular cation permeability due to a rare CLDN10B variant causes anhidrosis and kidney damage , 2017, PLoS genetics.

[4]  A. Paliege,et al.  AVP dynamically increases paracellular Na+ permeability and transcellular NaCl transport in the medullary thick ascending limb of Henle’s loop , 2016, Pflügers Archiv - European Journal of Physiology.

[5]  J. Hou,et al.  Mosaic expression of claudins in thick ascending limbs of Henle results in spatial separation of paracellular Na+ and Mg2+ transport , 2016, Proceedings of the National Academy of Sciences.

[6]  J. Hou,et al.  Corticomedullary difference in the effects of dietary Ca2+ on tight junction properties in thick ascending limbs of Henle’s loop , 2015, Pflügers Archiv - European Journal of Physiology.

[7]  J. Hou,et al.  Epigenetic regulation of microRNAs controlling CLDN14 expression as a mechanism for renal calcium handling. , 2015, Journal of the American Society of Nephrology : JASN.

[8]  D. Ellison,et al.  Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. , 2015, Cell metabolism.

[9]  N. Vázquez,et al.  Modulation of NCC activity by low and high K+ intake: insights into the signaling pathways involved , 2014, American journal of physiology. Renal physiology.

[10]  J. Hou,et al.  Claudin-14 underlies Ca⁺⁺-sensing receptor-mediated Ca⁺⁺ metabolism via NFAT-microRNA-based mechanisms. , 2014, Journal of the American Society of Nephrology : JASN.

[11]  A. Yu,et al.  Claudins and the modulation of tight junction permeability. , 2013, Physiological reviews.

[12]  J. Hoenderop,et al.  Increased expression of renal TRPM6 compensates for Mg2+ wasting during furosemide treatment , 2012, Clinical kidney journal.

[13]  T. Willnow,et al.  Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis , 2012, Proceedings of the National Academy of Sciences.

[14]  J. Hou,et al.  Claudin‐14 regulates renal Ca++ transport in response to CaSR signalling via a novel microRNA pathway , 2012, The EMBO journal.

[15]  Chou-Long Huang,et al.  The mechanism of hypocalciuria with NaCl cotransporter inhibition , 2011, Nature Reviews Nephrology.

[16]  D. Alessi,et al.  SORLA/SORL1 Functionally Interacts with SPAK To Control Renal Activation of Na+-K+-Cl− Cotransporter 2 , 2010, Molecular and Cellular Biology.

[17]  D. Günzel,et al.  Targeted deletion of murine Cldn16 identifies extra- and intrarenal compensatory mechanisms of Ca2+ and Mg2+ wasting. , 2010, American journal of physiology. Renal physiology.

[18]  J. Hou,et al.  Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium , 2009, Proceedings of the National Academy of Sciences.

[19]  M. Fromm,et al.  Claudin-10 exists in six alternatively spliced isoforms that exhibit distinct localization and function , 2009, Journal of Cell Science.

[20]  A. Yu,et al.  Function and regulation of claudins in the thick ascending limb of Henle , 2009, Pflügers Archiv - European Journal of Physiology.

[21]  Z. Abassi,et al.  Double gene deletion reveals lack of cooperation between claudin 11 and claudin 14 tight junction proteins , 2008, Cell and Tissue Research.

[22]  J. Hou,et al.  Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex. , 2008, The Journal of clinical investigation.

[23]  Sanae A. Kanzawa,et al.  Renal localization and function of the tight junction protein, claudin-19. , 2007, American journal of physiology. Renal physiology.

[24]  Stephan C F Neuhauss,et al.  Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement. , 2006, American journal of human genetics.

[25]  J. Hoenderop,et al.  Recent advances in renal tubular calcium reabsorption , 2006, Current opinion in nephrology and hypertension.

[26]  P. J. Kausalya,et al.  Disease-associated mutations affect intracellular traffic and paracellular Mg2+ transport function of Claudin-16. , 2006, The Journal of clinical investigation.

[27]  V. Vallon,et al.  Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia. , 2005, The Journal of clinical investigation.

[28]  R. Greger Cation selectivity of the isolated perfused cortical thick ascending limb of Henle's loop of rabbit kidney , 1981, Pflügers Archiv.

[29]  C. V. Van Itallie,et al.  Reversal of charge selectivity in cation or anion-selective epithelial lines by expression of different claudins. , 2003, American journal of physiology. Renal physiology.

[30]  D. Ellison,et al.  Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats. , 2003, American journal of physiology. Renal physiology.

[31]  V. Tasic,et al.  Novel paracellin-1 mutations in 25 families with familial hypomagnesemia with hypercalciuria and nephrocalcinosis. , 2001, Journal of the American Society of Nephrology : JASN.

[32]  S. Tsukita,et al.  Manner of Interaction of Heterogeneous Claudin Species within and between Tight Junction Strands , 1999, The Journal of cell biology.

[33]  F. S. Wright,et al.  Adaptation of the distal convoluted tubule of the rat. Structural and functional effects of dietary salt intake and chronic diuretic infusion. , 1989, The Journal of clinical investigation.