Fig. 1: PPARγ transcription factor regulates the expression of ACBP.
From: An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABAA receptor
A Heatmap representation of correlation (R) between ACBP mRNA and mRNA of several genes in the human liver, subcutaneous white adipose tissue (scWAT), and visceral white adipose tissue (viscWAT) (*p < 0.05). B Correlation plots of PPARG and ACBP mRNA in liver and WAT from human (liver: n = 179, visceral WAT: n = 355), mouse (liver: n = 179, epididymal WAT: n = 56), and rat (liver: n = 207, epididymal WAT: n = 47) extracts. Correlation plots of PPARG and ACBP mRNA in subcutaneous white adipose tissue (n = 442), skeletal muscle (n = 304), and the aggregate of all tissues (n = 7172) from human origin. C Venn diagram representation includes transcription factors (TFs) the targets of which are upregulated in bovine adipocytes, murine hepatocytes, and human leukocytes when their donors receive a high-fat diet (left). Significance of the upregulation of PPARγ target genes in each of the three datasets (right). D Chromatin immunoprecipitation sequencing (ChIP-seq) signals of PPARγ and H3K4me3 (Acbp promoter, mouse liver, n = 3). The black line corresponds to the peaks called per MACS. E Silencing of TFs encoding human ACBP in HepG2 cells. F Cytofluorometric peaks quantifying ACBP after silencing the unrelated negative control, ACBP, or PPARG (siUNR, siACBP, or siPPARG). G Heatmap representation of cytofluorometric ACBP protein levels upon silencing various TFs encoding ACBP in HepG2 cells (n = 3; one-way ANOVA). For statistical analyses (A, B) p values and R were calculated by Pearson and Spearman correlations respectively. See also Fig. S1.
