ReviewAmerican journal of physiology. Cell physiology2015
Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.
Review in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Ambroxol-Enhanced Frequency and Amplitude of Beating Cilia Controlled by a Voltage-Gated CaInternational journal of molecular sciences · 2023Article
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- Article
- Multiple molecular mechanisms are involved in the activation of the kidney sodium-chloride cotransporter by hypokalemia.Kidney international · 2022Article
- Intracellular ClInternational journal of molecular sciences · 2020Review
- Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule.Journal of the American Society of Nephrology : JASN · 2020Article
- NBCe1-A is required for the renal ammonia and KAmerican journal of physiology. Renal physiology · 2020Article
- Sympathetic regulation of NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats.American journal of physiology. Renal physiology · 2019Article
- Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake.Journal of the American Society of Nephrology : JASN · 2019Article
- The interplay of renal potassium and sodium handling in blood pressure regulation: critical role of the WNK-SPAK-NCC pathway.Journal of human hypertension · 2019Review
- Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter.Journal of the American Society of Nephrology : JASN · 2019Article
- Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Regulation of the renal NaCl cotransporter by the WNK/SPAK pathway: lessons learned from genetically altered animals.American journal of physiology. Renal physiology · 2019Article
- Kidney-specific WNK1 isoform (KS-WNK1) is a potent activator of WNK4 and NCC.American journal of physiology. Renal physiology · 2018Article
- Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel.Kidney international · 2018Article
- Role of the alternative splice variant of NCC in blood pressure control.Channels (Austin, Tex.) · 2018Review
- Pleiotropic Actions of FGF23.Toxicologic pathology · 2017Review
- Potassium Sensing by Renal Distal Tubules Requires Kir4.1.Journal of the American Society of Nephrology : JASN · 2017Article
- Potassium Homeostasis: The Knowns, the Unknowns, and the Health Benefits.Physiology (Bethesda, Md.) · 2017Review
- In Primary Aldosteronism, Mineralocorticoids Influence Exosomal Sodium-Chloride Cotransporter Abundance.Journal of the American Society of Nephrology : JASN · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renal thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC) is the salt transporter in the distal convoluted tubule. Its activity is fundamental for defining blood pressure levels. Decreased NCC activity is associated with salt-remediable arterial hypotension with hypokalemia (Gitelman disease), while increased activity results in salt-sensitive arterial hypertension with hyperkalemia (pseudohypoaldosteronism type II; PHAII). The discovery of four different genes causing PHAII revealed a complex multiprotein system that regulates the activity of NCC. Two genes encode for with-no-lysine (K) kinases WNK1 and WNK4, while two encode for kelch-like 3 (KLHL3) and cullin 3 (CUL3) proteins that form a RING type E3 ubiquitin ligase complex. Extensive research has shown that WNK1 and WNK4 are the targets for the KLHL3-CUL3 complex and that WNKs modulate the activity of NCC by means of intermediary Ste20-type kinases known as SPAK or OSR1. The understanding of the effect of WNKs on NCC is a complex issue, but recent evidence discussed in this review suggests that we could be reaching the end of the dark ages regarding this matter.
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