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. Author manuscript; available in PMC: 2021 Jan 7.
Published in final edited form as: Cell Metab. 2019 Nov 7;31(1):162–173.e5. doi: 10.1016/j.cmet.2019.10.003

Figure 6. TAZ interaction with PPARγ is regulated by Serine112 phosphorylation.

Figure 6.

(a) Co-immunoprecipitation of TAZ with PPARγ in eWAT. (b) Schematic representation of PPARγ depicting several protein domains, including PPYY motif and neighboring serine S112 phosphorylation site. (c) Inhibition of PPARγ S112 phosphorylation by MEK inhibitor PD98059 treatment decreases protein interaction with TAZ in 3T3-L1 adipocytes. (d) S112A phosphorylation of PPARγ by constitutively active (CA) ERK potentiates TAZ and PPARγ interaction in HEK293T cells. (e,f) Co-immunoprecipitation of TAZ and PPARγ WT, mutant S112D (e) or S112A (f) in HEK293T cells. (g) Effect of rosiglitazone treatment on interaction TAZ with PPARγ in differentiated 3T3-L1 adipocytes. (h) Transcriptional repression effect of TAZ on WT and S112A mutant PPARγ-driven gene transcription in dual-luciferase reporter assay in U2OS cells. Values are expressed as mean ± SEM. (e-g) n=3–4 *p< 0.05, **p< 0.01. See also figure S6.