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Literature DB >> 31371516

Reply to Farfel et al.: Is enhanced chloride reabsorption in proximal tubule a possible mechanism of metabolic acidosis in PHAII?

Jen-Chi Chen^1,2, Shih-Hua Lin¹, Chou-Long Huang³, Chih-Jen Cheng⁴.

Abstract

Entities: Chemical Disease

Year: 2019 PMID： 31371516 PMCID： PMC6697869 DOI： 10.1073/pnas.1910215116

Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205

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10 in total

1. Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins.

Authors: Kozue Yamauchi; Tatemitsu Rai; Katsuki Kobayashi; Eisei Sohara; Tatsunori Suzuki; Tomohiro Itoh; Shin Suda; Atsushi Hayama; Sei Sasaki; Shinichi Uchida
Journal: Proc Natl Acad Sci U S A Date: 2004-03-19 Impact factor: 11.205

2. KLHL3 regulates paracellular chloride transport in the kidney by ubiquitination of claudin-8.

Authors: Yongfeng Gong; Jinzhi Wang; Jing Yang; Ernie Gonzales; Ronaldo Perez; Jianghui Hou
Journal: Proc Natl Acad Sci U S A Date: 2015-03-23 Impact factor: 11.205

3. Familial hyperkalemia and hypertension and a hypothesis to explain proximal renal tubular acidosis.

Authors: Zvi Farfel; Haim Mayan; Steven J D Karlish
Journal: Proc Natl Acad Sci U S A Date: 2019-08-01 Impact factor: 11.205

4. WNK4 kinase is a physiological intracellular chloride sensor.

Authors: Jen-Chi Chen; Yi-Fen Lo; Ya-Wen Lin; Shih-Hua Lin; Chou-Long Huang; Chih-Jen Cheng
Journal: Proc Natl Acad Sci U S A Date: 2019-02-14 Impact factor: 11.205

5. A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis.

Authors: Karen I López-Cayuqueo; Maria Chavez-Canales; Alexia Pillot; Pascal Houillier; Maximilien Jayat; Jennifer Baraka-Vidot; Francesco Trepiccione; Véronique Baudrie; Cara Büsst; Christelle Soukaseum; Yusuke Kumai; Xavier Jeunemaître; Juliette Hadchouel; Dominique Eladari; Régine Chambrey
Journal: Kidney Int Date: 2018-07-07 Impact factor: 10.612

6. Pseudohypoaldosteronism type II: marked sensitivity to thiazides, hypercalciuria, normomagnesemia, and low bone mineral density.

Authors: Haim Mayan; Iris Vered; Meir Mouallem; Michal Tzadok-Witkon; Rachel Pauzner; Zvi Farfel
Journal: J Clin Endocrinol Metab Date: 2002-07 Impact factor: 5.958

Reply to Farfel et al.: Is enhanced chloride reabsorption in proximal tubule a possible mechanism of metabolic acidosis in PHAII?

1. Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins.

2. KLHL3 regulates paracellular chloride transport in the kidney by ubiquitination of claudin-8.

3. Familial hyperkalemia and hypertension and a hypothesis to explain proximal renal tubular acidosis.

4. WNK4 kinase is a physiological intracellular chloride sensor.

5. A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis.

6. Pseudohypoaldosteronism type II: marked sensitivity to thiazides, hypercalciuria, normomagnesemia, and low bone mineral density.

7. Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia.

Review 8. Electroneutral NaCl absorption in the proximal tubule: mechanisms of apical Na-coupled transport.

Review 9. Mechanisms in hyperkalemic renal tubular acidosis.

10. Mechanism of Hyperkalemia-Induced Metabolic Acidosis.