期刊
FEBS LETTERS
卷 581, 期 20, 页码 3887-3891出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2007.07.014
关键词
claudin-7; WNK4 kinase; phosphorylation; paracellular Cl- permeability; LLC-PK1 cells
Mutations in WNK4 have been linked to hypertension in PHAII. Paracellular ion transport has been reported to be involved in this disease process; however, the specific molecular target has not been identified. In this study, we found that TJ protein claudin-7 and WNK4 were partially co-localized in renal tubules of rat kidney and co-immunoprecipitated in kidney epithelial cells. The wild-type and PHAII-causing mutant, but not the kinase-dead mutant, phosphorylated claudin-7. We have identified ser(206) in the COOH-terminus of claudin-7 as a putative phosphorylation site for WNK4. More importantly, disease-causing mutant enhanced claudin-7 phosphorylation and significantly. increased paracellular permeability to Cl-. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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