Cellular mechanisms of WNK4-mediated regulation of ion transport proteins in the distal tubule

Gene mutations in WNK4 kinase cause a genetic form of hypertension by affecting multiple ion transport pathways through different mechanisms. Cai et al. report that the inhibitory effect of WNK4 on the thiazide-sensitive sodium-chloride cotransporter occurs through the lysosomal degradation pathway...

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Bibliographic Details
Published inKidney international Vol. 69; no. 12; pp. 2116 - 2118
Main Authors Peng, J.-B., Bell, P.D.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.06.2006
Elsevier Limited
Subjects
Animals
Carrier Proteins - analysis
Carrier Proteins - physiology
Humans
Hypertension - etiology
Hypertension - genetics
Hypertension - physiopathology
Ion Transport - physiology
Kidney Tubules, Distal - chemistry
Kidney Tubules, Distal - physiology
Lysosomes - drug effects
Lysosomes - physiology
Mutation
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - physiology
Pseudohypoaldosteronism - etiology
Pseudohypoaldosteronism - genetics
Pseudohypoaldosteronism - physiopathology
Signal Transduction - physiology
Sodium Chloride Symporters - analysis
Sodium Chloride Symporters - drug effects
Sodium Chloride Symporters - physiology
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Summary:Gene mutations in WNK4 kinase cause a genetic form of hypertension by affecting multiple ion transport pathways through different mechanisms. Cai et al. report that the inhibitory effect of WNK4 on the thiazide-sensitive sodium-chloride cotransporter occurs through the lysosomal degradation pathway in mammalian cells.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Commentary-1
ISSN:0085-2538
1523-1755
DOI:10.1038/sj.ki.5000435