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. 2013 Sep 17;4:253. doi: 10.3389/fphys.2013.00253

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Copyright © 2013 Richards, Jeffers, All, Cheng and Gumz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mutation of E-box elements inhibits basal and aldosterone-mediated αENaC promoter activity. (A) Cartoon of the αENaC promoter indicating E-box sites that were mutated and nearby hormone response elements (HRE) (not to scale). The position of each E-box element and HRE relative to the transcription start site is indicated. (B) Cells were transfected with the pRL renilla luciferase and a plasmid containing the αENaC promoter or a mutated form, cloned upstream of the firefly luciferase cDNA. E-box 1 (TCCAGCTGTC) at −1116, relative to the transcription start site was mutated to mE-box 1 (TCCAGCTAGC) and E-box 2 (TTCACCTGGG) at −116 was mutated to mE-box 2 (GGTACCTGGG). Cells were either not treated (No Tx) or treated with vehicle or aldosterone (aldo) for 24 h. Data are presented as the mean ± standard error, n = 6, ^**p < 0.01 vs. α ENaC/luc + no treatment.