Fig. 5: Blockage of T166 phosphorylation promotes PPARγ binding to lipid synthesis and accumulation-related gene loci. | Nature Communications

Fig. 5: Blockage of T166 phosphorylation promotes PPARγ binding to lipid synthesis and accumulation-related gene loci.

From: Lipid synthesis, triggered by PPARγ T166 dephosphorylation, sustains reparative function of macrophages during tissue repair

Fig. 5

a GO enrichment analysis showing the highly enriched metabolic pathway associated with WT or T166A PPARγ binding sites. b Binding peaks of WT or T166A PPARγ around indicated gene region. c ChIP-qPCR analysis of PPARγ binding to the Dbi, Plin2, Dgat1, Dgat2, Acly, Acaca and Fasn promoters in WT and T166A BMDMs. qPCR was performed with primers specific to the PPARγ-binding motifs. Data were normalized to the input. n = 3 biological replicates per group. d CUT&RUN qPCR of PPARγ binding to the indicated promoters in WT and T166A BMDMs (n = 3 biological replicates per group). Data were normalized to the spike in DNA. e The relative mRNA levels of FAS-related genes in WT or T166A BMDMs (n = 3 biological replicates per group) were assessed by RT-qPCR. f The relative mRNA levels of repair-related genes in WT or T166A BMDMs (n = 3 biological replicates per group) were assessed by RT-qPCR after treatment with IL-10 and C75 for 48 h. Unless specified otherwise, the data are presented as means ± s.e.m. (error bar) and compared using the two-tailed Student’s t test. Source data are provided as a Source Data file.

Back to article page