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Identification of Accessory Proteins Critical for the Epithelial Sodium Channel (ENaC)
Author(s) -
Horn Daniel,
Booth Rachell E
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.590.8
Subject(s) - epithelial sodium channel , pseudohypoaldosteronism , reabsorption , renal sodium reabsorption , microbiology and biotechnology , function (biology) , sgk1 , chemistry , biology , gene , sodium , endocrinology , biochemistry , kidney , kinase , organic chemistry
The epithelial sodium channel (ENaC) is rate‐limiting for the reabsorption of sodium in the distal nephron of the kidneys. Genetic mutations in ENaC can cause diseases such as Liddle's syndrome and pseudohypoaldosteronism type 1, causing severe hypertension or hypotension, respectively. Accessory proteins including Nedd4, ubiquitin protein‐ligase, and a serum and glucocorticoid‐regulated kinase have been shown to regulate ENaC and additional proteins are likely to play an essential role in its proper function. In an effort to identify proteins necessary for proper assembly, localization, and function of ENaC, BY4742 yeast deletion strains were transformed with αENaC, which induces a salt‐sensitive phenotype, and yeast dilution pronging assays were performed. While five deletion strains showed no effect on ENaC function in yeast, three strains lacking scj1 , jem1 , or lhs1 showed loss of ENaC function while deletion of ypk1 seemed to enhance ENaC function. Localization studies of αENaC in these deletion strains were used to elucidate the role of each gene on ENaC surface expression. Funded by NIH (R15GM086798) and Welch Foundation (Dept Grant A10048).