clearance from the target promoters. These studies thus establish an unexpected biological role for the CoREST complex, previously considered to mainly be involved in the repression of neuronal genes in NSCs or non-neuronal cells (Ballas et al., 2005). We also find that overexpression of Nurr77 and Nor1 in a macrophage cell line can suppress iNOS activation in response to LPS (K.S., unpublished), suggesting that the CoREST transrepression pathway may be widely used by members of the NR4A family. Of interest, reduction of most of the well-established components of the Co-REST complex severely compromises the anti-inflammatory activity of Nurr1. Quantitative defects in the expression or activities of these proteins could thus predispose certain organ systems to inflammation-sensitive pathologies, such as PD.
