ArticleProceedings of the National Academy of Sciences of the United States of America2003
WNK1, a kinase mutated in inherited hypertension with hyperkalemia, localizes to diverse Cl- -transporting epithelia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 132 citations in OpenAlex.
- Article
- Drosophila melanogaster: a simple genetic model of kidney structure, function and disease.Nature reviews. Nephrology · 2022Review
- A narrative review of Hyporeninemic hypertension-an indicator for monogenic forms of hypertension.Pediatric medicine (Hong Kong, China) · 2022Article
- WNKs are potassium-sensitive kinases.American journal of physiology. Cell physiology · 2021Article
- Advances in the development of novel compounds targeting cation-chloride cotransporter physiology.American journal of physiology. Cell physiology · 2021Review
- Article
- Pharmacological targeting of SPAK kinase in disorders of impaired epithelial transport.Expert opinion on therapeutic targets · 2017Review
- Regulatory Crosstalk by Protein Kinases on CFTR Trafficking and Activity.Frontiers in chemistry · 2016Review
- Gordon Syndrome: a continuing story.Pediatric nephrology (Berlin, Germany) · 2015Review
- Integrative network analysis reveals molecular mechanisms of blood pressure regulation.Molecular systems biology · 2015Article
- WNK1 activates large-conductance Ca2+-activated K+ channels through modulation of ERK1/2 signaling.Journal of the American Society of Nephrology : JASN · 2015Article
- Distal convoluted tubule.Comprehensive Physiology · 2015Review
- Comprehensive assessment of the association of WNK4 polymorphisms with hypertension: evidence from a meta-analysis.Scientific reports · 2014Article
- Mechanism and synergism in epithelial fluid and electrolyte secretion.Pflugers Archiv : European journal of physiology · 2014Review
- Comparative analysis of the expression profile of Wnk1 and Wnk1/Hsn2 splice variants in developing and adult mouse tissues.PloS one · 2013Article
- Bicarbonate promotes BK-α/β4-mediated K excretion in the renal distal nephron.American journal of physiology. Renal physiology · 2012Article
- In vivo Drosophilia genetic model for calcium oxalate nephrolithiasis.American journal of physiology. Renal physiology · 2012Article
- The WNK/SPAK and IRBIT/PP1 pathways in epithelial fluid and electrolyte transport.Physiology (Bethesda, Md.) · 2012Review
- Article
- WNK2 kinase is a novel regulator of essential neuronal cation-chloride cotransporters.The Journal of biological chemistry · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in WNK1 and WNK4, genes encoding members of a novel family of serine-threonine kinases, have recently been shown to cause pseudohypoaldosteronism type II (PHAII), an autosomal dominant disorder featuring hypertension, hyperkalemia, and renal tubular acidosis. The localization of these kinases in the distal nephron and the Cl(-) dependence of these phenotypes suggest that these mutations increase renal Cl(-) reabsorption. Although WNK4 expression is limited to the kidney, WNK1 is expressed in many tissues. We have examined the distribution of WNK1 in these extrarenal tissues. Immunostaining using WNK1-specific antibodies demonstrated that WNK1 is not present in all cell types; rather, it is predominantly localized in polarized epithelia, including those lining the lumen of the hepatic biliary ducts, pancreatic ducts, epididymis, sweat ducts, colonic crypts, and gallbladder. WNK1 is also found in the basal layers of epidermis and throughout the esophageal epithelium. The subcellular localization of WNK1 varies among these epithelia. WNK1 is cytoplasmic in kidney, colon, gallbladder, sweat duct, skin, and esophagus; in contrast, it localizes to the lateral membrane in bile ducts, pancreatic ducts, and epididymis. These epithelia are all notable for their prominent role in Cl(-) flux. Moreover, these sites largely coincide with those involved in the pathology of cystic fibrosis, a disease characterized by deranged epithelial Cl(-) flux. Together with the known pathophysiology of PHAII, these findings suggest that WNK1 plays a general role in the regulation of epithelial Cl(-) flux, a finding that suggests the potential of new approaches to the selective modulation of these processes.
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