کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2050649 | 1074176 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
WNK4 phosphorylates ser206 of claudin-7 and promotes paracellular Cl− permeability
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش گیاه شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: WNK4 phosphorylates ser206 of claudin-7 and promotes paracellular Cl− permeability WNK4 phosphorylates ser206 of claudin-7 and promotes paracellular Cl− permeability](/preview/png/2050649.png)
چکیده انگلیسی
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 ser206 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−.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: FEBS Letters - Volume 581, Issue 20, 7 August 2007, Pages 3887–3891
Journal: FEBS Letters - Volume 581, Issue 20, 7 August 2007, Pages 3887–3891
نویسندگان
Rodney Tatum, Yuguo Zhang, Qun Lu, Kwonseop Kim, Beverly G. Jeansonne, Yan-Hua Chen,