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. 2013 Jul 8;110(30):12331–12336. doi: 10.1073/pnas.1222684110

Fig. 3.

Fig. 3.

PER2 recruited corepressors to suppress OCT1-mediated TWIST1 promoter activity. (A) Diagram showing the five predicted OCT1 sites (Oct1-1–Oct1-5) on the TWIST1 promoter. (B and C) ChIP of PER2 (B) or OCT1 (C) on the TWIST1 promoter in MCF-10A cells. Normal IgG (IgG) and a site in 5′-UTR were used as controls for PER2-promoter association. (D) Coimmunoprecipitation (Co-IP) of PER2 and OCT1 in MCF-10A cells. Normal IgG was used as a control. (E) Immunoprecipitation of OCT1 or PER2 using MCF-10A nuclear extract (N.E.) and biotin-labeled oligonucleotides containing WT or mutated (mut) Oct1-5 site. (F and G) Relative fold change in luciferase activity of the TWIST1 reporter construct in HEK-293T cells transiently cotransfected with OCT1 or/and PER2 expression plasmids. Data show means ± SD. *P < 0.05 (Student t test). (H) Co-IP of PER2 and EZH2, SUZ12, HDAC2, Sin3A, or CoREST in MCF-10A cells. (Left) EZH2 and HDAC2 immunoblots were input images from the same blots with different exposure time. (I–L) ChIP of SUZ12 (I), EZH2 (J), trimethylated Histone 3 lysine 27 (H3K27me3) (K), and HDAC2 (L) in MCF-10A cells (SI Appendix, Figs. S4 and S5).