The role of the ENaC-regulatory complex in aldosterone-mediated sodium transport

Rama Soundararajan, David Pearce, Tim Ziera

Research output: Contribution to journalReview articlepeer-review

48 Scopus citations

Abstract

The mineralocorticoid aldosterone is indispensable for the control of blood pressure and fluid volume in mammals. It acts in large part to increase the abundance and activity of the epithelial Na + channel (ENaC), which mediates apical Na + entry in the distal parts of the kidney tubules. Aldosterone acts through the mineralocorticoid receptor to alter the transcription of specific genes, including SGK1 and GILZ1. Recent evidence suggests that these key aldosterone-regulated factors function within a unique multi-protein ENaC-regulatory-complex that governs the net cell surface expression and activity of the channel. Another aldosterone-induced protein, CNK3 (connector enhancer of kinase suppressor of Ras 3), also stimulates ENaC and has all of the features of a scaffolding protein. With these observations in mind, we discuss the possibility that CNK3 coordinates the dynamic assembly of the ENaC-regulatory-complex, and promotes context-appropriate aldosterone signal transduction in the regulation of epithelial Na + transport.

Original languageEnglish (US)
Pages (from-to)242-247
Number of pages6
JournalMolecular and cellular endocrinology
Volume350
Issue number2
DOIs
StatePublished - Mar 24 2012
Externally publishedYes

Keywords

  • Aldosterone signaling
  • ENaC-regulatory complex
  • Scaffold protein

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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