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. 2014 Mar 15;28(6):548–560. doi: 10.1101/gad.237081.113

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© 2014 Pekovic-Vaughan et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0.

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Figure 5. — Loss of rhythmic NRF2 pathway activity in Clock^Δ19 lungs. (A) Representative Western blots of diurnal NRF2 levels in total lung lysates from wild-type (WT) and Clock^Δ19 mice. NRF2 densitometry (mean ± SEM) was normalized to tubulin and expressed relative to wild-type ZT0. (*) P < 0.05 for wild type; not significant for Clock^Δ19, one-way ANOVA for the effect of time. (White bar) Light phase; (black bar) dark phase. (B) Temporal (ZT0 vs. ZT12) ChIP assays for the ARE regions of NRF2 targets (Gclm and Gsta3) in wild-type and Clock^Δ19 lungs using NRF2-specific antibody. Data (mean ± SEM) were expressed as percent input. (*) P < 0.05; (ns) not significant, t-test. (C) Temporal mRNA levels of Gclm and Gsta3 in wild-type and Clock^Δ19 lungs at ZT0 versus ZT12. Data (mean ± SEM) were normalized to Gapdh. (*) P < 0.05; (ns) not significant, t-test.