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• W1972659631 startingPage "204" @default.
• W1972659631 abstract "Liddle's syndrome is a form of inherited hypertension linked to mutations in the genes encoding the epithelial Na+ channel (ENaC). These mutations alter or delete PY motifs involved in protein-protein interactions with a ubiquitin-protein ligase, Nedd4. Here we show that Na+ transporting cells, derived from mouse cortical collecting duct, express two Nedd4 proteins with different structural organization and characteristics of ENaC regulation: 1) the classical Nedd4 (herein referred to as Nedd4-1) containing one amino-terminal C2, three WW, and one HECT-ubiquitin protein ligase domain and 2) a novel Nedd4 protein (Nedd4-2), homologous to Xenopus Nedd4 and comprising four WW, one HECT, yet lacking a C2 domain. Nedd4-2, but not Nedd4-1, inhibits ENaC activity when coexpressed in Xenopus oocytes and this property correlates with the ability to bind to ENaC, as only Nedd4-2 coimmunoprecipitates with ENaC. Furthermore, this interaction depends on the presence of at least one PY motif in the ENaC complex and on WW domains 3 and 4 in Nedd4-2. Thus, these results suggest that the novel suppressor protein Nedd4-2 is the regulator of ENaC and hence a potential susceptibility gene for arterial hypertension." @default.
• W1972659631 created "2016-06-24" @default.
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• W1972659631 date "2001-01-01" @default.
• W1972659631 modified "2023-10-03" @default.
• W1972659631 title "A novel mouse Nedd4 protein suppresses the activity of the epithelial Na⁺channel" @default.
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• W1972659631 doi "https://doi.org/10.1096/fj.00-0191com" @default.
• W1972659631 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11149908" @default.
• W1972659631 hasPublicationYear "2001" @default.
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