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. 2004 Jun;24(11):4651–4663. doi: 10.1128/MCB.24.11.4651-4663.2004

FIG. 7.

FIG. 7.

(A) PPARγ expression levels in differentiating 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were induced to differentiate. PPARγ expression levels were analyzed by Northern blotting. Ethidium bromide-stained 28S and 18S rRNA is shown as a control. (B to E) ChIP analysis of interactions on the PPARγ2 promoter as a function of time of differentiation of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were induced to differentiate and processed for ChIP assays at the indicated times. Portions of the PPARγ2 promoter or the β-actin gene were amplified from each sample. (B) Levels of interactions with C/EBPα, -β, and -δ. (C) Levels of interactions with tetra-acetylated H4 and K9-, K14-diacetylated H3. (D) Levels of interactions with TBP, TFIIB, TFIIH p89, and Pol II phosphorylated on Ser-5 of the CTD. (E) Levels of interactions with Brg1, Brm, and Ini1. Inset: linearity controls for PCR amplifications. Each ChIP was repeated in three to five independent experiments. The data shown in parts B, C, and E derive from a single differentiation experiment. ChIPs in part D derive from a different differentiation experiment.