ArticleKidney international2022
Multiple molecular mechanisms are involved in the activation of the kidney sodium-chloride cotransporter by hypokalemia.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Chloride at the spotlight-but not alone: towards a multi-ionic diuretic strategy.Clinical kidney journal · 2026Review
- Excess dietary potassium raises blood pressure in male mice by an aldosterone-dependent increase in ENaC.Communications biology · 2025Article
- NRBP1 and TSC22D proteins affect distal convoluted tubule physiology through modulation of the WNK pathway.Science advances · 2025Article
- NRBP1 and TSC22D proteins impact distal convoluted tubule physiology through modulation of the WNK pathway.bioRxiv : the preprint server for biology · 2024Article
- Arginine vasopressin regulates the renal NaAmerican journal of physiology. Renal physiology · 2024Article
- Expression of the kidney anion exchanger 1 affects WNK4 and SPAK phosphorylation and results in claudin-4 phosphorylation.Heliyon · 2023Article
- Markers of Kidney Tubular Function Deteriorate While Those of Kidney Tubule Health Improve in Primary Aldosteronism After Targeted Treatments.Journal of the American Heart Association · 2023Article
- The Integral Role of Chloride & With-No-Lysine Kinases in Cell Volume Regulation & Hypertension.International journal of nephrology and renovascular disease · 2023Review
- Potassium Homeostasis and WNK Kinases in the Regulation of the Sodium-Chloride Cotransporter: Hyperaldosteronism and Its Metabolic Consequences.Kidney360 · 2022Article
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15 authors at 5 institutions in 2 countries.
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Abstract
Low potassium intake activates the kidney sodium-chloride cotransporter (NCC) whose phosphorylation and activity depend on the With-No-Lysine kinase 4 (WNK4) that is inhibited by chloride binding to its kinase domain. Low extracellular potassium activates NCC by decreasing intracellular chloride thereby promoting chloride dissociation from WNK4 where residue L319 of WNK4 participates in chloride coordination. Since the WNK4-L319F mutant is constitutively active and chloride-insensitive in vitro, we generated mice harboring this mutation that displayed slightly increased phosphorylated NCC and mild hyperkalemia when on a 129/sv genetic background. On a low potassium diet, upregulation of phosphorylated NCC was observed, suggesting that in addition to chloride sensing by WNK4, other mechanisms participate which may include modulation of WNK4 activity and degradation by phosphorylation of the RRxS motif in regulatory domains present in WNK4 and KLHL3, respectively. Increased levels of WNK4 and kidney-specific WNK1 and phospho-WNK4-RRxS were observed in wild-type and WNK4
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