Fig. 4: p-T166 in the DBD modulates the transcriptional action of PPARγ. | Cell Death & Differentiation

Fig. 4: p-T166 in the DBD modulates the transcriptional action of PPARγ.

From: Blockage of PPARγ T166 phosphorylation enhances the inducibility of beige adipocytes and improves metabolic dysfunctions

Fig. 4

a–e Luciferase reporter assay evaluating the transcriptional activity of (a), WT, TA, and TD following treatment with vehicle or RSG; (b) WT, TA, and TD following treatment with vehicle or CDDO; (c) WT PPARγ under a gradient concentration of RSG; (d) Full-length or LBD-truncated PPARγ; (e) PRDM16 or PGC1α co-expressed with WT or mutant PPARγ. In (a–e), n = 3. f Co-immunoprecipitation of endogenous PPARγ with PRDM16 in PPARγ homozygous WT, TA, and TD SVF differentiated primary adipocytes. Experiments were repeated three times. g Co-IP analysis of the interaction between endogenous PPARγ and PGC1α in the three genotypes SVF differentiated primary adipocytes. Experiments were repeated three times. Data are expressed as the mean ± S.E.M. Data were analyzed by one-way ANOVA followed by Tukey’s test (a–e, f, g). *P < 0.05. **P < 0.01, ***P < 0.001.

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