To confirm whether CoREST was indeed localized to NF-κB target gene promoters in association with p65 and Nurr1, we performed ChIP assays of the iNOS- and TNFα-promoters in BV2 cells. The occupancy of NF-κB-p65, Nurr1 and CoREST on both the TNFα- and iNOS-promoters by all three proteins was strongly increased upon LPS stimulation (Fig. 4F, Fig. S9C). On the iNOS-promoter, which exhibits relatively slower activation kinetics, p65 binding preceded the binding of Nurr1, which in turn preceded recruitment of CoREST (Fig. 4F). To verify whether this system is indeed functional in vivo, we performed ChIP assays from microdissected SN after the stereotaxic injection of LPS into the SN. Consistent with in vitro data, Nurr1 is recruited to the iNOS- and TNFα–promoters after LPS stimulation (Fig. 4G, Fig. S9D). Finally, we asked whether Nurr1 was indeed essential for the recruitment of the CoREST complex to target gene promoters. ChIP experiments were performed using shNurr1- or shCtrl-BV2 cells. In the absence of Nurr1, CoREST was not recruited to the TNFα-promoter (Fig. 4H, left panel). Interestingly, under these conditions, p65 was present at
