Premium
Identification of Assessory Proteins Needed for ENaC Assembly and Function
Author(s) -
Rodrigues Roberta,
Ybanez Raquel,
Booth Rachell E
Publication year - 2012
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.26.1_supplement.867.18
Subject(s) - epithelial sodium channel , pseudohypoaldosteronism , renal sodium reabsorption , aldosterone , reabsorption , chemistry , endocrinology , medicine , homeostasis , microbiology and biotechnology , sodium , biology , kidney , organic chemistry
The epithelial sodium channel (ENaC) is a sodium transporting protein channel composed of three subunits, alpha, beta and gamma with a stoichiometric ratio of 1:1:1. ENaC regulates sodium reabsorption within the distal nephron and is essential for maintaining fluid homeostasis. ENaC dysfunction causes blood pressure disorders as seen with pseudohypoaldosteronism and Liddle's syndrome, which lead to hypotension and hypertension, respectively. Although there are several known activators and inhibitors of ENaC, including the sterol aldosterone and the peptide hormone arginine vasopressin, the role of other intracellular proteins affecting ENaC assembly is unclear. Our current studies utilize the yeast deletion strain library in conjunction with ENaC expression to identify accessory proteins that are crucial for ENaC assembly and function. Yeast strains expressing mouse ENaC demonstrate salt‐sensitivity (growth inhibition), while strains expressing ENaC and lacking SUR4, ERV1, EMP24 or ULA1 showed a reduction in salt‐sensitivity suggesting that they directly affect ENaC function or assembly. Supported by Research Corporation (CC6313) and NIH‐NIGMS (R15GM086798).