Extended Data Fig. 2: Effects of short-term triiodothyronine administration on ACBP/DBI expression.
From: Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing’s syndrome
(a-d) Cells were treated with siRNA targeting the thyroid hormone receptor (THR) α and β genes or control siRNA (siCtrl) and then cultured in the presence of triiodothyronine (T3). Then cells were subjected to the quantification of the mRNA coding for THRα, THRβ or ACBP (n=3/group; RU, relative units). (e) Scheme of T3 administration to female C57BL/6 mice for 16 h. (f) Plasma ACBP was assessed by ELISA after T3 treatment at different doses (n=6/group). (g) Liver Acbp mRNA levels (n=6/group; RU, relative units) after T3 treatment. (h) Representative immunoblot of ACBP after T3 treatment (n=3/group). β-actin was used as a loading control. (i) Scatter plot showing the ACBP/β-actin ratio. One-way ANOVA with Tukey correction was used for statistical analysis (P-values are indicated). All dot plots indicate means ± SEM.
