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. Author manuscript; available in PMC: 2009 Oct 3.
Published in final edited form as: Cell. 2009 Apr 3;137(1):47–59. doi: 10.1016/j.cell.2009.01.038

Fig. 6. The CoREST complex is required for Nurr1-mediated repression in astrocytes.

Fig. 6

A. Effect of IL1β stimulation on association of Nurr1 and p65 in mouse primary astrocytes. Lysates of astrocytes stimulated with IL1β for the indicated times were immunoprecipitated with anti-Nurr1 antibody and Western blots were developed with anti-p65 antibody. B. Recruitment of Nurr1 and p65 to iNOS-promoter in mouse primary astrocyte shown by ChIP assay. Data represent fold enrichment of iNOS- promoter precipitated with the indicated antibodies compared to control IgG as determined by qPCR. C. Effect of GSK3β-specific inhibitor SB21 on recruitment of Nurr1 to iNOS-promoter. Data represent fold enrichment of iNOS-promoter precipitated with antibody against Nurr1 compared to control IgG as determined by qPCR. D. Interaction of Nurr1 and CoREST in mouse primary astrocytes. Co-IP was performed with anti-Nurr1 antibody and Western blots developed with anti-CoREST or anti-Nurr1 antibodies. E. Recruitment of Nurr1 and CoREST to iNOS-promoter in mouse primary astrocytes shown by ChIP assay. Data represent fold enrichment of iNOS-promoter precipitated with the indicated antibodies compared to control IgG as determined by qPCR. F–H. Effect of knockdown of the components of CoREST-repressor complex on mRNAs encoding inflammatory mediators. Mouse primary astrocytes were infected with lentivirus carrying shRNA against CoREST, LSD1, G9a, HDAC1 or control. Cells were stimulated with IL1β for 6h and mRNA expression of iNOS (F), CSF1 (G) and Ncf1 (H) was determined by qPCR. I. Nurr1-dependent clearance of p65 from iNOS promoter. ChIP assay was performed in shNurr1- or shCtrl-astrocyte and data shown as fold enrichment over control IgG of iNOS promoter precipitated with antibody against p65.