Figure 6.
Dexamethasone increases ESRRB expression and binding to GR-regulated genes. (A) The human T-ALL cell lines DND-41 and KOPTK1 were treated with dexamethasone for 6 hours, and ESRRB expression was quantified in nuclear lysates by immunoblot analysis with an ESRRB antibody. ESRRB protein levels were quantified by densitometry. ESRRB bound GC target genes in dexamethasone-sensitive (KOPTK1) but not dexamethasone-resistant (CUTLL1) human T-ALL cells. (B-D) The schematics (top) show putative ERRE sites in introns of GR target genes. ChIP (bottom) was performed with an ESRRB antibody or an IgG control, and DNA was quantified by qPCR and the ΔΔCT method, with primers to the putative ESRRB binding sites. The percentage input was normalized to IgG control. The results are averages of 3 independent experiments; error bars represent SEM. *P < .05; **P < .01.

Dexamethasone increases ESRRB expression and binding to GR-regulated genes. (A) The human T-ALL cell lines DND-41 and KOPTK1 were treated with dexamethasone for 6 hours, and ESRRB expression was quantified in nuclear lysates by immunoblot analysis with an ESRRB antibody. ESRRB protein levels were quantified by densitometry. ESRRB bound GC target genes in dexamethasone-sensitive (KOPTK1) but not dexamethasone-resistant (CUTLL1) human T-ALL cells. (B-D) The schematics (top) show putative ERRE sites in introns of GR target genes. ChIP (bottom) was performed with an ESRRB antibody or an IgG control, and DNA was quantified by qPCR and the ΔΔCT method, with primers to the putative ESRRB binding sites. The percentage input was normalized to IgG control. The results are averages of 3 independent experiments; error bars represent SEM. *P < .05; **P < .01.

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