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Article

WNK4 inhibition of ENaC is independent of Nedd4-2-mediated ENaC ubiquitination.

American journal of physiology. Renal physiology - 1 Jul 2013

Yu Ling, Cai Hui, Yue Qian, Alli Abdel A, Wang DeXuan, Al-Khalili Otor, Bao Hui-Fang, Eaton Douglas C

Abstract excerpt

A serine-threonine protein kinase, WNK4, reduces Na⁺ reabsorption and K⁺ secretion in the distal convoluted tubule by reducing trafficking of the thiazide-sensitive Na-Cl cotransporter to and enhancing renal outer medullary potassium channel retrieval from the apical membrane. Epithelial sodium channels (ENaC) in the distal nephron also play a role in regulating Na⁺ reabsorption and are also regulated by WNK4,...

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Source

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Identifiers

PMID: 23594824
DOI: 10.1152/ajprenal.00652.2012
PMCID: PMC3725674

Genes

WNK4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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WNK4 inhibition of ENaC is independent of Nedd4-2-mediated ENaC ubiquitination.PMID 23594824Read ↗

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Regulation of the Na-K-2Cl cotransporter NKCC2 by ubiquitylationSemantic proximity Read ↗

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WNK4, as thiazides, shuts off NaCl reabsorption to stimulate Na/K exchange.Semantic proximity Read ↗

Role of WNK kinases in regulating tubular salt and potassium transport and in the development of hypertension.Semantic proximity Read ↗

WNK4 regulates activity of the epithelial Na+ channel in vitro and in vivo.Semantic proximity Read ↗

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