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Updated: Aug 8, 2026

Polysome Fractionation and Analysis of Mammalian Translatomes on a Genome-wide Scale
Published on: May 17, 2014
Translational regulation of Na-K-ATPase subunit mRNAs by glucocorticoids
1Pediatric Nephrology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. pdevaraj@aecom.yu.edu
Abstract:
Glucocorticoids (GC) regulate Na-K-ATPase-subunit mRNA transcription. However, GC-induced increases in Na-K-ATPase activity are not always paralleled by changes in subunit mRNA abundance. We therefore examined posttranscriptional mechanisms of subunit gene regulation by GC. cDNA-derived mRNAs encoding alpha 1-, alpha 3-, and beta 1-subunits were tested for stability and translation efficiency in a cell-free lysate, in the presence of hydrocortisone (HC) or dexamethasone (Dex). No effect of HC on subunit mRNA stability was noted. Translation efficiency of alpha1- and alpha 3-mRNAs, but not of beta 1-mRNA, was significantly increased by HC and Dex. Deletion of the 5'untranslated region (5'UT) of alpha 1-mRNA abolished this effect. Translation of a chimeric beta 1-mRNA, constructed by transposing the 5'UT of alpha 1 onto the coding region of beta1, was enhanced by HC. Transposition of a putative steroid-modulatory element conserved in the 5'UT of all alpha isoforms (ACAGGACCC) onto the coding region of beta 1-mRNA rendered it responsive to HC. A synthetic primer containing the ACAGGACCC sequence abolished the effect of HC on alpha 1- and chimeric beta 1-mRNAs. Our results indicate that GC can directly enhance Na-K-ATPase translation in vitro in a subunit-specific manner, via a putative GC-modulatory element situated in a predicted loop structure within the 5'UT of alpha-mRNAs.
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