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Editorial
. 2013 Oct 1;305(7):F968-9.
doi: 10.1152/ajprenal.00386.2013. Epub 2013 Jul 10.

Aldosterone-dependent trans-activation and epigenetic derepression of ENaC: where is the balance?

Affiliations
Editorial

Aldosterone-dependent trans-activation and epigenetic derepression of ENaC: where is the balance?

Alexander Staruschenko. Am J Physiol Renal Physiol. .
No abstract available

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Figures

Fig. 1.
Fig. 1.
Simplified model for the aldosterone-sensitive regulation of α-epithelial Na+ channel (ENaC) expression. Af9 directly binds +78/+92 of the α-ENaC promoter and recruits Dot1a to this position to basally repress α-ENaC transcription. Aldosterone relieves this repression by dispersing the Dot1a-Af9 complex from the α-ENaC promoter, prompting histone H3 Lys79 hypomethylation that induces α-ENaC transcription. In contrast, Sp1 binding to a +222/+229 cis-element of the α-ENaC promoter contributes significantly as a basal driver of α-ENaC, acting independently from and overcoming the Dot1a-Af9 repressor complex. In addition, aldosterone further enhances Sp1 occupancy of the α-ENaC promoter.

Comment on

References

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